Neurocritical Care Triad - Focused NeurologicalExamination, Brain Multimodal Monitoring and

Maintaining Neuro Homeostasis

ww.sciencedirect.com

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0

Available online at w

journal homepage: www.elsevier .com/locate/apme

Research Article

Neurocritical care triad e Focused neurologicalexamination, brain multimodal monitoring andmaintaining 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, Indiab Professor of Neurology, Institute of Neurology, Madras Medical College, Chennai 600003, Tamil Nadu, IndiacSenior 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

* Corresponding author. 3/5 Subhiksha Sai KE-mail address: lakshmineuro@gmail.com

0976-0016/$ e see front matter Copyright ªhttp://dx.doi.org/10.1016/j.apme.2013.08.010

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 limited scope for clinical examination in view of altered

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

ribha, Sri Krishnapuram(R. Lakshmi Narasimha

2013, Indraprastha Medic

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

Street, Royapettah, Chennai 600014, India.n).al Corporation Ltd. All rights reserved.

Table 1 e Brain stem reflexes.

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0194

irreversible so, the focus of neurocritical care is to prevent,

detect and manage SBI.1

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

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).

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

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.

Themost 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.

NEURO CRITICAL

CARE

FOCUSSED NEUROLOGICAL EXAMINATION

BRAIN MULTIMODAL MONITORING

NEURO HOMEOSTASIS

Fig. 1 e Neurocritical care triad.

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. ElectroencephalographyIn 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 electroencephalographyQuantitative 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

Table 2 e Five P’s of focused neurological examination.

Pupillary response

Pattern of breathing

Posturing

Paucity of limb movements

Plantar response

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

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0 195

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 potentialsAcoustic 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 pressureICP 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

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

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-zeroedwhenever needed and can

be used to drain CSF in case of ICP. The placement of these

monitors varies and depends on the site of themaximal injury

in focal lesions. In diffuse injury, the monitor is usually posi-

tioned in the frontal lobe of the non-dominant hemisphere.

Thesemonitors are placed through small burr hole, which can

Table 5 e Some commonly used scales in neurocriticalcare.

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)

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

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0196

also be used for placing the other intraparenchymalmonitors,

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 andmass 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>20mmHg (sensitivitye 95%, specificitye 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

Fig. 2 e Normal ICP wave.

which is either tunneled or placed through amultilumen 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 ameasure 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 extremeswere

associated with worse outcome in patients with traumatic

brain injury. SjvO2 complements focal monitoring of PbtO2.1

2.2.6. Regional cerebral blood flowCBF is a measure of blood supply to the brain in a given time.

Even though PbtO2 is a goodmarker of CBF, it does not provide

a direct dimension of CBF as it is influenced by other param-

eters. Recently, directmeasure 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 microdialysisCMD 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 60min) 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

CPP

THERAPY

INTRACRANIAL COMPLIANCE

DYNAMICITY

HEMODYNAMIC STATUS

AUTO REGULATION

Fig. 4 e Factors influencing CPP.

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0 197

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 vasoconstrictioncascade (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 mmHg. 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 hemodynamicmaneuvers 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.

Therapeutic

target to

Increase CPP

Increased

Vasoconstriction

Decreased CBF

DECREASED ICP

--> decrease in

Edema

Fig. 3 e CPP therapy by vasoconstriction cascade.

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 allowingmargin 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.

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 � 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

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0198

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

Fig. 5 e Schematic approach in

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. FeverThe 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.

management of raised ICP.

Table 8 e Characteristics comparison between CSW andSIADH.

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

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0 199

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. EuglycemiaHyperglycemia, which is a common scenario in neurologically

critical patients exerts its deleterious effect by free radical for-

mation, activationofN-Methyl D-aspartate receptors, triggering

of apoptotic and inflammatory pathways, increased intracel-

lular calcium and altered lactatemetabolismwith 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 imbalanceHyponatremia 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

withoutaknownstimulus leads toprimarynatriuresis leadingto

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 insipidusIt is characterized by excessive thirst alongwith excess amount

of dilute urine. Deficiency of ADH is the main pathogenesis.

Normally ADH acts by increasing water permeability in collect-

ingductsanddistal tubulesactingmainly inAquaporin2protein

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.

This isattainedbyanalyzing thedifferenceofabsorptionspectra

of oxygenated and deoxygenated hemoglobin and cytochrome

aa3. The concurrent monitoring of transmittance across the

human brain at two ormore wavelengths enables alterations of

optical attenuationof thespectra tobeconverted intochangesof

cerebral oxygenation.11 NIRS by coalescing with indocyanine

green dye dilutionmight 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.

r e f e r e n c e s

1. Hemphill J Claude, Andrews Peter, De Georgia Michael.Multimodal monitoring and neurocritical care bioinformatics.Nat Rev Neurol. 2011;7:451e460.

2. Goldstein Joshua N, Greer David M. Rapid focusedneurological assessment in the emergency department andICU. Emerg Med Clin North Am. 2009;27:1e16.

3. Chang Andrew K, Shinnar Shlomo. Nonconvulsive statusepilepticus. Emerg Med Clin North Am. 2011;29:65e72.

4. Wijdicks EF, Worden WR, Miers A, Piepgras DG. The earlydays of the neurosciences intensive care unit. Mayo Clin Proc.2011;86(9):903e906.

a p o l l o m e d i c i n e 1 0 ( 2 0 1 3 ) 1 9 3e2 0 0200

5. Oddoa Mauro, Villab Federico, Citeriob Giuseppe. Curr OpinCrit Care. 2012;18:111e118.

6. Jordan KG. Continuous EEG monitoring in the neuroscienceintensive care unit and emergency department. J ClinNeurophysiol. 1999;16:14e39.

7. Chiappa KH, Hill RA. Evaluation and prognostication in coma.Electroencephalogr Clin Neurophysiol. 1998;106:149e155.

8. White Hayden, Cook David, Venkatesh Bala. The use ofhypertonic saline for treating intracranial hypertension.Anesth Analg. 2006;102:1836e1846.

9. Brandi G, Bechir M, Sailer S, et al. Transcranial color-codedduplexsonographyallows toassesscerebralperfusionpressurenoninvasively following severe traumatic brain injury.2010;152(6):965e972.

10. Rajajee V, Fletcher J, Rochlen LR, et al. Comparison ofaccuracy of optic nerve ultrasound for detection ofintracranial hypertension. Crit Care. 2012;16(3):R79.

11. Wartenberg Katja Elfriede, Schmidt J Michael, Mayer StephanA. Multimodality monitoring in neurocritical care. Crit CareClin. 2007;23:507e538.

12. Carter LP, Weinand ME, Oommen KJ. Cerebral blood flow(CBF) monitoring in intensive care by thermal diffusion. ActaNeurochir. 1993;59:43e46.

13. Marshall Scott A, Kalanuria Atul. The management ofintracerebral pressure in the neurosciences critical care.Neurosurg Clin N Am. 2013.

14. Rangel-Castillo Leonardo, GopinathShankar, RobertsonClaudiaS. Management of intracranial hypertension. Neurol Clin.2008;26(2):521e541.

15. Marcoux KK. Management of increased intracranial pressurein the critically ill child with an acute neurological injury.AACN Clin Issues. 2005;16(2):212e231.

16. Shibata M. Hyperthermia in brain hemorrhage. MedHypotheses. 1998;50:185e190.

17. Busto R, Dietrich WD, Globus MY, et al. Small differences inintraischemic brain temperature critically determine theextent of ischemic neuronal injury. J Cereb Blood Flow Metab.1987;7:729e738.

18. Wass CT, Lanier WL, Hofer RE, et al. Temperature changes of> or ¼1 degree C alter functional neurologic outcome andhistopathology in a canine model of complete cerebralischemia. Anesthesiology. 1995;83:325e350.

19. Kramer Andreas H, Roberts Derek J, Zygun David A. Crit Care.2012;16.

20. Keller E, Wolf M, Martin M, et al. Estimation of cerebraloxygenation and hemodynamics in cerebral vasospasm usingindocyaninegreendyedilutionandnear infrared spectroscopy:a case report. J Neurosurg Anesthesiol. 2001;13(1):43e48.

21. Terborg C, Bramer S, Harscher S, et al. Bedside assessment ofcerebral perfusion reductions in patients with acute ischaemicstroke by near-infrared spectroscopy and indocyanine green. JNeurol Neurosurg Psychiatry. 2004;75(1):38e42.

Apollo hospitals: http://www.apollohospitals.com/Twitter: https://twitter.com/HospitalsApolloYoutube: http://www.youtube.com/apollohospitalsindiaFacebook: http://www.facebook.com/TheApolloHospitalsSlideshare: http://www.slideshare.net/Apollo_HospitalsLinkedin: http://www.linkedin.com/company/apollo-hospitalsBlog:Blog: http://www.letstalkhealth.in/