Intensive care is rightly described as “an art of managing intense intricacy” and this situation is further complicated in the care of patients with critical neurological illness. Brain damage directly related to an insult is primary brain injury (PBI). The cascade of pathobiological events following PBI is known as secondary brain injury (SBI). PBI is most often irreversible so, the focus of neurocritical care is to prevent, detect and manage SBI.

1. Neurocritical Care Triad - Focused Neurological
Examination, Brain Multimodal Monitoring and
Maintaining Neuro Homeostasis

2. Research Article
Neurocritical care triad e Focused neurological
examination, brain multimodal monitoring and
maintaining neuro homeostasis
R. Lakshmi Narasimhan a,b,
*, N. Praveen Chander c
, R. Ravichandran c
,
P. Venkatesh c
a
Senior Consultant, Apollo Hospitals, Chennai, Tamil Nadu, India
b
Professor of Neurology, Institute of Neurology, Madras Medical College, Chennai 600003, Tamil Nadu, India
c
Senior Registrar, Institute of Neurology, Madras Medical College, Chennai 600003, Tamil Nadu, India
a r t i c l e i n f o
Article history:
Received 7 August 2013
Accepted 8 August 2013
Available online 2 September 2013
Keywords:
Neurocritical care
Focused neurological examination
Brain multimodal monitoring
Neuro homeostasis
a b s t r a c t
Intensive care is rightly described as “an art of managing intense intricacy” and this sit-
uation is further complicated in the care of patients with critical neurological illness. Brain
damage directly related to an insult is primary brain injury (PBI). The cascade of patho-
biological events following PBI is known as secondary brain injury (SBI). PBI is most often
irreversible so, the focus of neurocritical care is to prevent, detect and manage SBI. The
quintessential of neurocritical care is focused neurological assessment, appropriate neu-
roimaging and real time monitoring targeted at preserving neuro homeostasis. Focused
neurological assessment includes a rapid examination of brain stem reflexes, five P’s,
identifying nonconvulsive status epilepticus and using appropriate assessment scales.
Brain multimodal monitoring is employed to assess and follow the trends in intracranial
pressure, brain tissue oxygenation, regional cerebral blood flow and EEG. This helps in
critical decision making. SBI characterized by a series of cellular injury cascades and other
secondary insults deranges the neuro homeostasis. Maintaining CPP, treating fever, good
glycemic control and appropriate management of electrolyte imbalances are the corner-
stones in mitigating the secondary insult to the brain.
Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
1. Introduction
Intensive care is rightly described as “an art of managing
intense intricacy” and this situation is further complicated in
the care of patients with critical neurological illness owing to
limited scope for clinical examination in view of altered
conscious levels.
Brain damage directly related to an insult is primary brain
injury (PBI). The cascade of pathobiological events following
PBI is known as secondary brain injury (SBI). PBI is most often
* Corresponding author. 3/5 Subhiksha Sai Kribha, Sri Krishnapuram Street, Royapettah, Chennai 600014, India.
E-mail address: lakshmineuro@gmail.com (R. Lakshmi Narasimhan).
Available online at www.sciencedirect.com
journal homepage: www.elsevier.com/locate/apme
a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3 e2 0 0
0976-0016/$ e see front matter Copyright ª 2013, Indraprastha Medical Corporation Ltd. All rights reserved.
http://dx.doi.org/10.1016/j.apme.2013.08.010

3. irreversible so, the focus of neurocritical care is to prevent,
detect and manage SBI.1
2. Triad of neurocritical care
Quintessential of neurocritical care is focused neurological
assessment, appropriate neuroimaging and real time moni-
toring targeted at preserving neuro homeostasis (Fig. 1).
2.1. Focused neurological examination
Focused neurological examination in caring a critically ill pa-
tient with neurological illness is a paradigm shift from the
conventional detailed neurological assessment in the primary
care setting as it is extremely time sensitive and the mental
state of the patient often does not permit a reliable clinical
judgment.2
The key is to craft an efficient and focused eval-
uation without compromising on the accuracy in diagnosis
and delay in initiating appropriate treatment.
The most crucial and decisive aspect in the examination of
patient presenting with impaired consciousness is the
assessment of brain stem reflexes (Table 1). This helps in
distinguishing between brain stem and diffuse cerebral
dysfunction as a cause of the impairment. This is followed by
assessment of asymmetry in neurological examination which
when present points to a focal cause like an infraction, he-
matoma or abscess. We recommend looking for five P’s
(Table 2) which aids in the rapid assessment.
Raised intracranial pressure (ICP) presents with various
herniation syndromes which can be recognized by their
characteristic signs (Table 3).
Detecting nonconvulsive status epilepticus (NCSE) is a
challenge because of its subtle manifestations. NCSE consti-
tutes 25% of all cases of status epilepticus and 58% of cases do
not have a previous history of epilepsy.3
It is a heterogeneous
disorder including absence SE (ASE), complex partial SE (CPSE)
and subtle SE (SSE). Clinical features and key facts about NCSE
are summarized in Table 4.
Skin lesions which are likely to be missed may provide
significant clues to the diagnosis. This includes rashes, es-
chars, lesion in the genitalia and marks of intravenous drug
abuse.
Several standardized assessment scales are available
which assist in uniform grading of disease severity and pre-
dicting the prognosis in neurocritical care. Few commonly
used scales are listed in Table 5.
2.2. Brain Multimodality Monitoring (BMM)
BMM targets at a wide range analysis of the injured human
brain tissue. In addition to the benefit of monitoring of critical
deviations, the physiological parameters are also used to
guide therapy4
(Table 6).
It is amalgamation of brain physiological data derived from
various parameters like intracranial pressure (ICP), cerebral
perfusion pressure (CPP), brain tissue oxygen (PbtO2), cerebral
microdialysis (CMD) and electroencephalography (EEG)
monitoring of brain function.5
2.2.1. Electroencephalography
In spite of continuous brain monitoring, subclinical seizures
are detected only by EEG. EEG is sensitive to brain ischemia
and can also detect neuronal dysfunction at an early revers-
ible stage.
2.2.2. Quantitative electroencephalography
Quantitative EEG converts the EEG signal into a wide range of
amplitude and frequency measurements which can be easily
interpreted by non-EEG experts. These are reproduced in vi-
sual display compatible forms, as bar graphs, scalp maps or
compressed spectral arrays. They are used to discriminate
involuntary movements from seizures which is a common
diagnostic dilemma in NICU.6
NEURO
CRITICAL
CARE
FOCUSSED
NEUROLOGICAL
EXAMINATION
BRAIN
MULTIMODAL
MONITORING
NEURO
HOMEOSTASIS
Fig. 1 e Neurocritical care triad.
Table 1 e Brain stem reflexes.
Reflex Assessment
Pupillary Asses direct and consensual pupillary
response to light
Corneal Closure of eyelid following stimulation
of cornea
Grimace Facial movement in response to supraorbital
ridge or temporomandibular joint
Oculocephalic Conjugate movement of eyes opposite to the
direction head turn.
Oculovestibular Caloric test e tonic deviation and nystagmus
of eyes in response to irrigation of ears with
cold and warm water. Direction of nystagmus
(C-O/W-S : Cold water e Opposite side/Warm
water e Same side)
Gag Elevation of soft palate in response to
stimulation of pharyngeal mucosa
Table 2 e Five P’s of focused neurological examination.
Pupillary response
Pattern of breathing
Posturing
Paucity of limb movements
Plantar response
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4. Bispectral Index (BIS): The BIS is a complex but empirical
measurement, which are statistically derived from large
database of EEGs. It helps in continuous monitoring of the
level of consciousness, especially in patients under sedation.
2.2.3. Evoked Potentials (EP) and event-related potentials
Acoustic EP, somatosensory EP, motor EP are used in NICU
settings to test vision, hearing, and motor function as clinical
assessment is not reliable in patients with altered
consciousness.7
The importance and utility of acoustic EP testing in pa-
tients at risk of peripheral damage (infections, temporal bone
fractures, antibiotics) have been established. The absence of
cortical somatosensory EPs is one of the primary indicator in
predicting poor prognosis in post anoxic patients. Motor EPs
represent a sensitive and specific tool for monitoring
descending motor tracts in predicting the outcome in acute
cerebral lesions.
2.2.4. Intracranial pressure
ICP monitoring can be used to prognosticate the course of
various intracranial diseases. It also aids in assessing the
other global perfusion metrics like CPP. The factors that in-
fluence the pathophysiology of intracranial hypertension are
mechanism of cerebral edema, volume of intracranial com-
ponents, integrity of the blood/brain barrier (BBB), and CPP.
The BBB forms a semi permeable membrane which in accor-
dance with the equilibrium of the transcapillary hydrostatic
pressure gradient counterbalanced by osmotic pressure
gradient (Starling’s forces) which determines the extent of
flow into brain substance.8
ICP waveform (Fig. 2) can be monitored by invasive moni-
toring devices which include the extraventricular drain (EVD),
intraparenchymal fiber-optic monitor, subdural bolt, and
epidural fiber-optic catheters. These devices can be easily
placed technically and can record pressure continuously. The
technology used in these monitors varies, and they can
incorporate fiber-optic, strain gauge, or pneumatic technolo-
gies. The gold standard device for monitoring ICP is a ven-
tricular catheter which is attached to an external micro-strain
gauge. This device can be re-zeroed whenever needed and can
be used to drain CSF in case of ICP. The placement of these
monitors varies and depends on the site of the maximal injury
in focal lesions. In diffuse injury, the monitor is usually posi-
tioned in the frontal lobe of the non-dominant hemisphere.
These monitors are placed through small burr hole, which can
Table 3 e Herniation syndromes.
Site of herniation Vessels occluded Structures compressed Clinical manifestations
Falcine/cingulate Ant. cerebral art.
Great cerebral vein
Cingulate cortex under falx cerebri
and thalamus/basal ganglia
- Lower extremity weakness
- Sensory loss
- Apraxia, abulia, akinetic mutism
- Trans cortical motor aphasia
- Urinary incontinence
Uncal/tentorial
herniation
Ipsilateral post. cerebral artery Ipsilateral 3rd nerve
Uncus
Contralateral cerebral peduncles
(Kernohan’s notch syndrome)
Ipsi. 3rd nerve palsy
Ipsi. dilated pupil with Ipsi. hemiparesis
Central/
trans tentorial
Medial perforating branches
of basilar art.
Brain stem
Ipsi/bilateral 6th nerve
Decreased consciousness
Bilateral/unilateral 6th nerve palsy
Foraminal herniation Post. inferior cerebellar arteries
Vertebral arteries
Medulla
Brain stem
Impending death
Table 4 e Nonconvulsive status epilepticus.
Type Clinical manifestations
Subtle generalized Coma with subtle or no motor manifestations
Complex partial Confusional state, usually with automatisms
Absence Continuous or fluctuating confusion
Consider NCSE if
- Prolonged postictal period
- Stroke patients who look clinically worse than expected
- Coma or altered sensorium of undetermined cause
Major clues to the diagnosis of NCSE
- Abrupt onset
- Fluctuating mental status
- Subtle clinical signs such as eye fluttering, lip smacking,
and picking movements with fingers
Table 5 e Some commonly used scales in neurocritical
care.
Level-of-consciousness Glasgow coma scale
Full Outline Unresponsiveness e
FOUR score
Delirium scale Confusion Assessment Method (CAM)
Richmond Agitation Sedation Scale
(RASS)
Stroke deficit scales NIH stroke scale
Canadian neurological scale
Assessment of motor
function
Fugl-Meyer
Motor assessment scale
Mobility assessment Rivermead mobility index
Balance assessment Berg balance assessment
Measures of disability Barthel index
Functional Independence Measure
(FIM)
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5. also be used for placing the other intraparenchymal monitors,
such as brain tissue oxygen monitors or microdialysis probes.
The other popular method to monitor ICP is an intra-
parenchymal fiber-optic device. Through a cranial bolt it is
inserted as a bedside procedure, thus less technically chal-
lenging. This device displays ICP waveform continuously. The
risk of bleeding and infections is less when compared to the
ventricular catheters. The only concern is that, it cannot be re-
zeroed and thus cannot be used to drain CSF.8
Among the non-invasive methods two options considered
now are Pulsality Index (PI) and optic nerve sheath diameter
(ONSD).
PI which can estimate ICP non-continuously, is determined
by TransCranial Doppler (TCD). Ipsilateral/contra lateral PI
ratio >1.25 indicates compartmentalized ICP and mass effect.9
The USG guided assessment of ONSD is done by placing a
linear array probe over the superolateral margin of orbit with
angulation towards medially. An ONSD greater than 0.48 cm
denotes ICP >20 mm Hg (sensitivity e 95%, specificity e 93%).8,10
2.2.5. Brain tissue oxygen tension (PbtO2)
PbtO2 measures the balance between regional oxygen supply
and its use. It is measured by a small flexible microcatheter
which is either tunneled or placed through a multilumen bolt.
The catheter is inserted into the brain parenchyma in a given
area of interest usually in the hypoperfused area as deter-
mined by imaging perfusion studies. The catheter is usually
passed through gray matter to white matter, for effective data
comparison between the areas. Normally a tissue volume of
17 mm3
is measured. Normal PbtO2 value depends on the re-
gion under scrutiny. It is usually high in areas such as cortex
and hippocampus (with high density of neurons) and lower in
white matter.11
PbtO2 less than 15 mm Hg is associated with
poor outcome in patients with TBI.
Jugular venous oxygen saturation (SjvO2) is measured by a
small fiber-optic catheter placed in the internal jugular vein
with the tip advanced to the jugular bulb. SjvO2 is a measure of
global cerebral oxygen extraction. SjvO2 less than 50% in-
dicates ‘ischemic desaturations’ whereas a value of more than
75% represents luxury perfusion and both these extremes were
associated with worse outcome in patients with traumatic
brain injury. SjvO2 complements focal monitoring of PbtO2.1
2.2.6. Regional cerebral blood flow
CBF is a measure of blood supply to the brain in a given time.
Even though PbtO2 is a good marker of CBF, it does not provide
a direct dimension of CBF as it is influenced by other param-
eters. Recently, direct measure of rCBF is possible via a thermal
diffusion probe (TDP) that is inserted into brain parenchyma
along with ICP/PbtO2 probes. The probe has two thermistors,
Proximal one is set to tissue temperature, whereas the distal
one is 2
C above the tissue temperature. The tissue’s ability to
dissipate heat is determined by the distal thermistor: the
greater the CBF, greater the dissipation of heat. This informa-
tion is converted into a measure of CBF in ml/100 g/min.1,12
Muench et al used TDP to guide medical therapy of delayed
cerebral ischemia in SAH patients; and showed that CBF can be
improved by vasopressors significantly, whereas hemodilution
and hypervolemia had only marginal effects.5
2.2.7. Cerebral microdialysis
CMD is a process by which a specialized catheter tipped with a
semi permeable dialysis membrane (with a 20 kDa cutoff), is
inserted in the brain parenchyma. The catheter is continuously
perfused with a CSF-like solution, which allows regular (usu-
ally every 60 min) sampling of patients’ brain extracellular fluid
into microvials and bedside analysis using manufacturer’s
device. This allows on-line monitoring of dynamic changes in
patients’ neurochemistry [mainly glucose, lactate/pyruvate
ratio (LPR), glutamate] which provides important information
on the adequacy of brain energy supply and cellular function.5
After cerebral ischemia, a pattern of elevated glutamate,
elevated LPR or low glucose is a sign of cellular hypoxia. These
variations may precede alterations in standard brain physio-
logic variables and thus therapies can be administered earlier.
2.3. Maintaining neuro homeostasis
SBI characterized by a series of cellular injury cascades and
other secondary insults deranges the neuro homeostasis.
Cellular injury cascades include initiation free radicals,
intracellular calcium influx, excititoxicity, ischemic cascades
etc. Secondary brain insults occur due to decreased supply of
Table 6 e Neurocritical care physiological parameters.
Parameters Values
Brain parameters
ICP 20 mm Hg
Brain tissue oxygen tension 15 mm Hg
Jugular venous oxygen
saturation
55e75%
Cerebral blood flow 55 ml/100 g/min (global);
z25 ml/100 g/min
(white matter)
Lactate:pyruvate
concentration ratio
40
General parameters
Systolic BP 90 mm Hg
MAP 80
Systemic arterial oxygen
saturation
94%
End-tidal carbon dioxide
concentration
35e40 mm Hg
Heart rate 80e100
Respiratory rate 12e16 breaths/min
Fig. 2 e Normal ICP wave.
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6. substrates which is very much disproportionate to the
increased demand, thus compromising on the compensatory
mechanisms. Such insults can occur in seizures, fever, hy-
perglycemia etc.
2.3.1. Cerebral Perfusion Pressure (CPP)
CPP is the driving force for blood flow across cerebral micro-
vascular capillary bed.
CPP [ MAP L ICP. The normal CPP is between 60 and
70 mm Hg. CPP could be augmented by
- Decreasing ICP
- Increasing MAP.
2.3.1.1. Principle of CPP targeted therapy e vasoconstriction
cascade (Fig. 3). The compensatory vasoconstriction leads to
reduced cerebral blood flow and thereby reduced ICP. How-
ever this compensatory mechanism is effective only with
intact autoregulation. CPP target is tailored in different pa-
tients depending on the degree of autoregulation, intracranial
compliance, dynamicity and hemodynamic status. For
example if the patient’s autoregulation is impaired, then tar-
geting a higher CPP (70) is deleterious (produces pulmonary
edema) rather than producing beneficial effects (Fig. 4).
The main treatment goal is to maintain ICP 20 cm of H2O or
15 mm Hg. Current guidelines recommend measures to con-
trol ICP when pressures of 20 mm Hg are reached, and to use
aggressive means to prevent ICP more than 25 mm Hg or CPP
60 mm Hg. CPP goes hand in hand with ICP as the concept is
to maintain CPP along with ICP in the optimal range for a
better outcome in critically ill patients. Awareness of this is
important because hemodynamic maneuvers to lower ICP can
also lower CPP which can be deleterious.13
2.3.1.2. Resection of mass lesions. Intracranial space occu-
pying lesions producing elevated ICP needs to be removed
whenever possible. Acute epidural and subdural hematomas
are surgical emergency. Brain abscess ought to be drained,
and pneumocephalus must be evacuated.
2.3.1.3. Hyperosmolar therapy. There are essentially two
types of cerebral edema namely cytotoxic and vasogenic
edema.
1. Cytotoxic edema is linked with cell death leading to failure
of ion homeostasis. Intracellular ischemia and hypoxia
leads to cytotoxic edema which leads to cell death. Intra-
cellular swelling occurs and both gray and white matter
edema occurs in imaging.
2. Vasogenic edema results from breakdown of the bloode-
brain barrier. It is extracellular edema appearing mostly in
the white matter. It is mostly associated with neoplasms or
cerebral abscesses.
Usually cerebral edema occurs as a combination of both.
In both the situation hyperosmolar therapy is effective. In
cytotoxic edema, osmotic therapy may reduce the volume of
normal brain surrounding the lesion allowing margin of safety
by decreasing ICP. Steroids and surgical resection of lesion,
though is the mainstay of treatment osmotic therapy also has
beneficial role.
The characteristic of ideal osmotic agent is to establish a
strong transendothelial osmotic gradient by remaining in the
intravascular compartment. It should be inert, nontoxic, and
has minimal systemic side effects. Both mannitol and hy-
pertonic saline (HTS) fulfills these criteria, with HTS in upper
hand8
(Table 7).
2.3.1.4. Hyperventilation. It is a temporary means to curb
raised ICP. It is the choice of treatment esp. in case of hyper-
emia. Prolonged hyperventilation can be deleterious as it can
produce cerebral ischemia. Duration advised is usually 12 h
and PCO2 is maintained from 30 to 35 and not less than
25 mm Hg.
Therapeutic
target to
Increase CPP
Increased
Vasoconstriction
Decreased CBF
DECREASED ICP
-- decrease in
Edema
Fig. 3 e CPP therapy by vasoconstriction cascade.
CPP
THERAPY
INTRACRANIAL
COMPLIANCE
DYNAMICITY
HEMODYNAMIC
STATUS
AUTO
REGULATION
Fig. 4 e Factors influencing CPP.
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7. 2.3.1.5. Sedation and analgesia. Agitation and pain which is
commonly encountered in NICU setting can significantly in-
crease ICP which can be mitigated by adequate sedation and
analgesia. In such settings, benzodiazepines and narcotics
can be used, among which the former is a better choice. Short
acting drugs are commonly used in order to assess neurolog-
ical status intermittently.14
2.3.1.6. Decompressive Craniectomy (DC). DC has been used in
treating uncontrolled IC hypertension. A part of the calvaria is
removed to create a window which acts as an access for the
brain to expand thus preventing herniation thereby negating
MonroeKellie doctrine.
2.3.1.7. Barbiturate coma. This is administered only for re-
fractory intracranial hypertension considering the serious
adversities of high-dose barbiturates. Pentobarbital is given as
loading dose of 10 mg/kg weight which is followed by 5 mg/kg
body weight hourly for 3 doses. A dose is 1e2 mg/kg/h, is used
as maintenance adjusted to serum level of 30e50 mg/ml or
until the EEG shows a burst suppression pattern14
(Fig. 5).
2.3.1.8. Methods to increase MAP
- Fluid management e fluids should be administered so as to
establish either euvolemia or moderate hypervolemia. Col-
loids and crystalloids are used for this purpose. Pulmonary
capillary wedge pressure of 12e15 mm Hg and central
venous pressure of 8e10 mm Hg are the target to be main-
tained. Packed red cells are also used as volume expanders.
- Vasopressors e Phenylephrine can be used to increase the
CPP. Dosage of 40e80 mg/250 ml of 0.9% NaCl can be used.
Norepinephrine (4 mg/250 ml 0.9% NaCl) at a maximum
dosage of 0.2e0.4 mcg/kg per minute has become the
standard vasopressors. Alternatively Inj. Dopamine can
also be used to maintain CPP. Care should be taken not to
raise the CPP above 70 mm Hg as it can lead to ARDS.
- Flat positioning e placing the patients head in a flat po-
sition, helped in maintaining CPP. However ICP can be
mildly elevated. Certain studies show that placing the
patient at 15e30
can lead to an optimum CPP as well as
low ICP.15
2.3.2. Fever
The optimum body temperature is mediated in the hypo-
thalamus, which regulates the balance between production
and conservation of heat. The thermal energy produced by the
visceral organs and tissues is the main source of heat in the
body and is known as obligatory thermogenesis.
Thermogenesis through voluntary muscular and
behavioral activity as well as involuntary autonomic sys-
tem activity is called as facultative thermogenesis. Heat
also may be gained passively by conduction and convection
from the environment, when ambient temperature exceeds
body temperature, and by radiation from solar or other
sources.
Table 7 e Characteristics comparison between HTS and mannitol.
HTS Mannitol
Sustenance of the osmotic gradient e
determined by reflection co-efficient
Greater e more potent osmotic drug Lesser
CPP e by increasing MAP as CPP ¼ MAP À ICP Z/normal ; can reduce MAP
Immunomodulation Has a role e by reducing adhesion of
leukocytes to endothelium
e
BBB integrity Maintained Not maintained e can cross BBB
Restoration of neuronal membrane potential Present Absent
Fig. 5 e Schematic approach in management of raised ICP.
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8. 2.3.2.1. Fever and neuronal injury. Experimental studies show
that hyperthermia has a detrimental effect on the brain.16,17
Even a temperature increase of 1
C or 1.2
C can results in
permanent neuronal loss especially after an ischemic insult.18
2.3.2.2. Benefits of lowering brain temperature. Hypothermia
reduces the release of excitotoxic neurotransmitters, helps in
diminishing the oxidative stress, preserves the integrity of the
BBB with attenuation of cerebral edema, decreases post
ischemic inflammatory reactions, maintains acid-base sta-
bility in the brain, and helps restore protein synthesis. Overall
it also decreases cerebral metabolism along with reduced
consumption of oxygen and glucose.
2.3.3. Euglycemia
Hyperglycemia, which is a common scenario in neurologically
critical patients exerts its deleterious effect by free radical for-
mation, activationof N-Methyl D-aspartatereceptors, triggering
of apoptotic and inflammatory pathways, increased intracel-
lular calcium and altered lactate metabolism with reduction in
pH. Concurrently Hypoglycemia can also be deleterious
because neurologically ill patients are entirely dependent on
glucose as an energy source for CNS. Thus even moderate
reduction in glucose can lead to severe neuroglycopenia.
Through many studies it has been proved that, intensive
insulin therapy is of no benefit in improving the mortality of
neurocritical care patients. More harmful effects are caused
due to sugar levels 200 mg/dl. Thus the target goal has to be
between 110 and 180 mg/dl e (euglycemic) state for a better
outcome.19
2.3.4. Electrolyte imbalance
Hyponatremia is the commonest electrolyte imbalance
encountered in NICU with intracranial pathologies especially
SAH. Among the other causes of hyponatremia, SIADH, Cerebral
Salt Wasting (CSW) syndrome is frequently present. Both share
common features and are difficult to distinguish. CSW, which
withoutaknownstimulusleadstoprimarynatriuresisleadingto
hyponatremia and hypovolemia.
It is due increased plasma volume that distends atria walls,
a sympathetic stimulus, or the increased angiotensin, which
increases the release of the natriuretric peptides, mostly Brain
natriuretric peptides. This leads to diminished activity of the
Renin Angiotensin Aldosterone system and an increased
natriuresis in the distal tubule. In neurologically injured pa-
tients it is important to distinguish between CSW and SIADH
(Table 8).
2.3.5. Central diabetes insipidus
It is characterized by excessive thirst along with excess amount
of dilute urine. Deficiency of ADH is the main pathogenesis.
Normally ADH acts by increasing water permeability in collect-
ing ducts anddistal tubules actingmainlyinAquaporin2 protein
channels / water reabsorption and concentrated urine. Since
the ADH production from posterior Pituitary is affected, the
normal mechanisms are altered leading to the condition.
3. Future trends
Near infrared spectroscopy (NIRS) is a non-invasive technique
employed to determine regional cerebral oxygen saturation.
Thisisattainedby analyzing the difference ofabsorptionspectra
of oxygenated and deoxygenated hemoglobin and cytochrome
aa3. The concurrent monitoring of transmittance across the
human brain at two or more wavelengths enables alterations of
optical attenuation of the spectra tobe converted into changes of
cerebral oxygenation.11
NIRS by coalescing with indocyanine
green dye dilution might be used to detect and treat the cerebral
vasospasm in SAH20
thus preventing delayed cerebral ischemic
insult. The same technique is also to assess the perfusion ab-
normalities in acute ischemic strokes.21
4. Summary
Neurocritical care with the triad of focal neurological exami-
nation, multimodal monitoring of brain and maintaining the
neuro homeostasis shall prevent secondary brain injury,
thereby improving the quality of life in patients suffering from
cerebral catastrophes.
Conflicts of interest
All authors have none to declare.
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Table 8 e Characteristics comparison between CSW and
SIADH.
CSW SIADH
Plasma volume Z /normal
Salt balance Negative Variable
Water balance Negative /normal
Dehydration Present Absent
Central venous
pressure
Z /normal
Serum osmolality Z Z
Urine sodium
Urine volume Z/normal
Hematocrit /normal Normal
Plasma bun/
creatinine
/normal Z
Treatment Normal saline/
hypertonic saline/
fludrocortisone
Fluid restriction/
frusemide/hypertonic
saline/democycline
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