Neurocritical Care Triad - Focused Neurological
Examination, Brain Multimodal Monitoring and
Maintaining Neuro Homeostasis
Research Article
Neurocritical care triad e Focused neurological
examination, brain multimodal monitoring and
maintaining ...
irreversible so, the focus of neurocritical care is to prevent,
detect and manage SBI.1
2. Triad of neurocritical care
Qui...
Bispectral Index (BIS): The BIS is a complex but empirical
measurement, which are statistically derived from large
databas...
also be used for placing the other intraparenchymal monitors,
such as brain tissue oxygen monitors or microdialysis probes...
substrates which is very much disproportionate to the
increased demand, thus compromising on the compensatory
mechanisms. ...
2.3.1.5. Sedation and analgesia. Agitation and pain which is
commonly encountered in NICU setting can significantly in-
cre...
2.3.2.1. Fever and neuronal injury. Experimental studies show
that hyperthermia has a detrimental effect on the brain.16,1...
5. Oddoa Mauro, Villab Federico, Citeriob Giuseppe. Curr Opin
Crit Care. 2012;18:111e118.
6. Jordan KG. Continuous EEG mon...
Apollohospitals:http://www.apollohospitals.com/
Twitter:https://twitter.com/HospitalsApollo
Youtube:http://www.youtube.com...
Upcoming SlideShare
Loading in …5
×

Neurocritical Care Triad - Focused Neurological Examination, Brain Multimodal Monitoring Andamaintaining Neuro Homeostasis

937 views
859 views

Published on

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.

Published in: Health & Medicine
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
937
On SlideShare
0
From Embeds
0
Number of Embeds
0
Actions
Shares
0
Downloads
19
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide

Neurocritical Care Triad - Focused Neurological Examination, Brain Multimodal Monitoring Andamaintaining Neuro Homeostasis

  1. 1. Neurocritical Care Triad - Focused Neurological Examination, Brain Multimodal Monitoring and Maintaining Neuro Homeostasis
  2. 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. 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 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 0194
  4. 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) 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 0 195
  5. 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. 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 0196
  6. 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. 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 0 197
  7. 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. 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 0198
  8. 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. 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 focused neurological assessment in the emergency department and ICU. Emerg Med Clin North Am. 2009;27:1e16. 3. Chang Andrew K, Shinnar Shlomo. Nonconvulsive status epilepticus. Emerg Med Clin North Am. 2011;29:65e72. 4. Wijdicks EF, Worden WR, Miers A, Piepgras DG. The early days of the neurosciences intensive care unit. Mayo Clin Proc. 2011;86(9):903e906. 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 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 0 199
  9. 9. 5. Oddoa Mauro, Villab Federico, Citeriob Giuseppe. Curr Opin Crit Care. 2012;18:111e118. 6. Jordan KG. Continuous EEG monitoring in the neuroscience intensive care unit and emergency department. J Clin Neurophysiol. 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 of hypertonic saline for treating intracranial hypertension. Anesth Analg. 2006;102:1836e1846. 9. Brandi G, Be´chir M, Sailer S, et al. Transcranial color-coded duplex sonographyallowsto assesscerebral perfusionpressure noninvasively following severe traumatic brain injury. 2010;152(6):965e972. 10. Rajajee V, Fletcher J, Rochlen LR, et al. Comparison of accuracy of optic nerve ultrasound for detection of intracranial hypertension. Crit Care. 2012;16(3):R79. 11. Wartenberg Katja Elfriede, Schmidt J Michael, Mayer Stephan A. Multimodality monitoring in neurocritical care. Crit Care Clin. 2007;23:507e538. 12. Carter LP, Weinand ME, Oommen KJ. Cerebral blood flow (CBF) monitoring in intensive care by thermal diffusion. Acta Neurochir. 1993;59:43e46. 13. Marshall Scott A, Kalanuria Atul. The management of intracerebral pressure in the neurosciences critical care. Neurosurg Clin N Am. 2013. 14. Rangel-Castillo Leonardo, Gopinath Shankar, Robertson Claudia S. Management of intracranial hypertension. Neurol Clin. 2008;26(2):521e541. 15. Marcoux KK. Management of increased intracranial pressure in the critically ill child with an acute neurological injury. AACN Clin Issues. 2005;16(2):212e231. 16. Shibata M. Hyperthermia in brain hemorrhage. Med Hypotheses. 1998;50:185e190. 17. Busto R, Dietrich WD, Globus MY, et al. Small differences in intraischemic brain temperature critically determine the extent 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 and histopathology in a canine model of complete cerebral ischemia. 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 cerebral oxygenation and hemodynamics in cerebral vasospasm using indocyanine green dye dilution and near infrared spectroscopy: a case report. J Neurosurg Anesthesiol. 2001;13(1):43e48. 21. Terborg C, Bramer S, Harscher S, et al. Bedside assessment of cerebral perfusion reductions in patients with acute ischaemic stroke by near-infrared spectroscopy and indocyanine green. J Neurol Neurosurg Psychiatry. 2004;75(1):38e42. 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 0200
  10. 10. Apollohospitals:http://www.apollohospitals.com/ Twitter:https://twitter.com/HospitalsApollo Youtube:http://www.youtube.com/apollohospitalsindia Facebook:http://www.facebook.com/TheApolloHospitals Slideshare:http://www.slideshare.net/Apollo_Hospitals Linkedin:http://www.linkedin.com/company/apollo-hospitals Blog:Blog:http://www.letstalkhealth.in/

×