Critical care in neurology

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Critical care in neurology

  1. 1. Flying PublisheR#72012Kitchener, Hashem, Wahba,Khalaf, Zarif, MansoorCritical Carein NeurologyFlying Publisher Guide totheMore books at www.FlyingPublisher.comgoo.gl/QOUDJ
  2. 2. Kitchener – Hashem – Wahba – Khalaf – Zarif – MansoorCritical Care in Neurology
  3. 3. Nabil KitchenerSaher HashemMervat WahbaMagdy KhalafBassem ZarifSimin MansoorThe Flying Publisher Guide toCritical Care in Neurology2012 EditionFlying Publisher
  4. 4. 4 |Correspondence:nabilkitchener@consultant.comDisclaimerNeurocritical care is an ever-changing field. The publishers andauthor of The Flying Publisher Guide to Critical Care inNeurology have made every effort to provide information that isaccurate and complete as of the date of publication. However, inview of the rapid changes occurring in medical science, as wellas the possibility of human error, this site may contain technicalinaccuracies, typographical or other errors. It is theresponsibility of the reading physician who must rely onexperience and knowledge about the patient to determine thebest treatment and care pathway. The information containedherein is provided “as is”, without warranty of any kind. Thecontributors to this book, including Flying Publisher & Kamps,disclaim responsibility for any errors or omissions or for resultsobtained from the use of information contained herein.This work is protected by copyright both as a whole and in part.Copy editing: Nilly Nagy and Rob Camp© 2012 by Flying Publisher & Kamps / Design: Attilio BaghinoISBN: 978-3-942687-07-2
  5. 5. | 55PrologueNeurointensive care is a relatively new field that has developedas a subspecialty of critical care and neurology. The goal ofneurointensive care, and the neurointensivist, is to treat andprevent primary and secondary brain (or other nervous system)injury. Inherent in this goal are the monitoring tools unique tothe neurointensive care unit, including the most basic butperhaps the most important tool, the neurologic examination. Inthe era of the subspecialty of critical care neurology, theneurologist is working now as an aggressive interventionalistwho manages life-threatening disorders of the nervous system.The neurointensivist’s role is to help follow the neurologic statusand treat the patient while integrating his/her knowledge ofother organ systems and expertise in critical care, to provide themost comprehensive care possible for the patient.Critical care neurology is practiced in emergency rooms, inconsultations in general medical and surgical intensive careunits, in intermediary care units such as stroke units, and inspecialized neurointensive care units where patients arefrequently on life-support systems involving ventilators,intravascular lines, and monitoring and treatment devices. Datahas shown that care provided by clinicians specializing inneurologic injury, and within dedicated neurointensive careunits, improves patient functional outcome, and reduceshospital mortality, length of stay and resource utilization.This book emphasizes the clinical and practical aspects ofmanagement in the neurointensive care unit.This book is written, mainly, for the neurologist working in, ordirecting, a specialized neurointensive care unit(neurointensivists), as well as other specialists including strokeneurologists, neurosurgeons, pulmonary/critical care specialists,anesthesiologists, nurse practitioners, critical care registered
  6. 6. 6 |nurses, and therapists all working together towards improvedneurologic recovery.We hope this book can provide a new addition to the emergingliterature of critical care neurology, and heighten therecognition by general medical and surgical intensivists of theimportance and complexities of nervous system dysfunction incritically ill and injured patients.The EditorsNabil Kitchener, Saher Hashem, Mervat WahbaEgypt, USA, January 2012
  7. 7. 7 |EditorsNabil Kitchener, MD, PhDProfessor of Neurology, GOTHI,EgyptPresident of Egyptian Cerebro-Cardio-Vascular Association(ECCVA) and Board Director ofWorld Stroke Organization(WSO)www.ECCVA.comnabilkitchener@consultant.comSaher Hashem, MDProfessor and Chairman ofNeurology and NeurocriticalDepartmentCairo University, EgyptMervat Wahba, MD, FCCPAssistant Professor of NeurologyDepartment of NeurologyUniversity of Tennessee HealthSciences Center, UTHSC, USAAuthorsMagdy Khalaf, MDConsultant Neurologist andChairman of Neurocritical CareUnitGOTHI, EgyptBassem Zarif, MDLecturer of CardiologyNational Heart Institute, GOTHI,EgyptSimin Mansoor, MDDepartment of NeurologyUniversity of Tennessee HealthSciences Center, UTHSC, USA
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  9. 9. | 9Table of Contents1. Assessment of Patients in Neurological Emergency............... 13History...................................................................................... 15Physical Exam.......................................................................... 161. Mental status................................................................... 162. Cranial nerve (CN) exam................................................ 163. Motor exam ..................................................................... 184. Reflexes............................................................................ 185. Sensory exam.................................................................. 186. Coordination and balance ............................................. 187. Neuroanatomical localization....................................... 19Conclusions .............................................................................. 202. How to Approach an Unconscious Patient .............................. 21Diagnosis .................................................................................. 23Basic assessments............................................................... 24General Care of the Comatose Patient.................................. 27Permanent Vegetative State.................................................. 27Diagnosis.............................................................................. 29Management ....................................................................... 29Locked-in Syndrome............................................................... 30Brain Death .............................................................................. 313. Documentation and Scores........................................................ 32Scoring and Documentation .................................................. 34Delirium.................................................................................... 38
  10. 10. 10 |4. Brain Injuries............................................................................... 39Types of Brain Injuries ........................................................... 39Primary brain injuries ....................................................... 39Secondary brain injuries ................................................... 42Management of Special Issues............................................... 44Traumatic brain injury ...................................................... 44Acute stroke ........................................................................ 45Status epilepticus (SE)........................................................ 46Neuromuscular emergencies ............................................ 47Management of subarachnoid hemorrhage.................... 505. Basic Hemodynamic Monitoring of Neurocritical Patients... 536. Neurocritical Monitoring........................................................... 59Neuro-Specific Monitoring .................................................... 59Clinical Assessment................................................................. 60The Glasgow Coma Scale.................................................... 60Pupillary response.............................................................. 60Invasive Monitoring................................................................ 61Measuring ICP..................................................................... 62Indications for ICP monitoring......................................... 62Intracranial Pressure Waveforms and Analysis.............. 63Jugular Venous Oximetry (SjvO2)...................................... 67Brain Tissue Oximetry ....................................................... 69Noninvasive Monitoring......................................................... 71Continuous measures of CBF by Transcranial Doppler.. 71Near Infrared Spectroscopy .............................................. 73Electrophysiological Monitoring........................................... 73Application of the EEG in the ICU:.................................... 76Multimodal Monitoring.......................................................... 77Conclusions .............................................................................. 777. Cerebral Edema........................................................................... 79Types of Cerebral Edema........................................................ 81Management of Cerebral Edema ........................................... 82
  11. 11. | 118. General Neurological Treatment Strategies............................ 84Swallowing Disturbances ....................................................... 85Respiratory Management in Neurocritical Care ................. 86Infection Control in Neurocritical Care................................ 89Pain Relief and Sedation......................................................... 90Bedside approach to the agitated patient ....................... 91Role of Rehabilitation ............................................................. 92Diagnostic Findings in Cerebral Death ................................. 93Conclusion................................................................................ 969. Medical Diseases and Metabolic Encephalopathies................ 97Examination of the Encephalopathic Patient...................... 98General Pathophysiology ....................................................... 99Hepatic Encephalopathy ........................................................ 99Complications of hepatic encephalopathy (HE) ........... 100Treatment of hepatic encephalopathy .......................... 102Renal Encephalopathies ....................................................... 102Fluid and Electrolyte Imbalance.......................................... 104Osmolarity disorders........................................................ 104Encephalopathy in Diabetic Patients.................................. 106Hypoxic Ischemic Encephalopathy (HIE) ........................... 107Septic Encephalopathy ......................................................... 108Drug-induced Encephalopathies ......................................... 10810. References.................................................................................. 109
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  13. 13. Assessment of Patients in Neurological Emergency | 131. Assessment of Patients inNeurological EmergencyNabil Kitchener, Saher HashemCare in specialized intensive care units (ICUs) is generally ofhigher quality than in general care units. Neurocritical carefocuses on the care of critically ill patients with primary orsecondary neurosurgical and neurological problems and wasinitially developed to manage postoperative neurosurgicalpatients. It expanded thereafter to the management of patientswith traumatic brain injury (TBI), intracranial hemorrhage andcomplications of subarachnoid hemorrhage; includingvasospasm, elevated intracranial pressure (ICP) and thecardiopulmonary complications of brain injury.Neurocritical care units have developed to coordinate themanagement of critically ill neurological patients in a singlespecialized unit, which includes many clinical domains. Care isprovided by a multidisciplinary team trained to recognize anddeal with the unique aspects of the neurological diseaseprocesses, as several treatable neurological disorders arecharacterized by imminent risk of severe and irreversibleneurological injury or death if treatment is delayed.Some diseases need immediate action, so admission to the NICUis the best solution when there is:
  14. 14. 14 | Critical Care in Neurology1) Impaired level of consciousness.2) Progressive respiratory impairment or the need formechanical ventilation in a neurological patient.3) Status epilepticus or prolonged seizures.4) Clinical or Computed Tomographic (CT) evidence of raisedIntracranial Pressure (ICP), whatever the cause (spaceoccupying lesion, cerebral edema or hemorrhagicconversion of a cerebral infarct, intracerebral hemorrhage,etc.)5) Need for monitoring (for example, level of consciousness,ICP, continuous electroencephalography (cEEG)), and6) Need for specific treatments (Baldwin 2010) (e.g.,neurosurgery, intravenous or arterial thrombolysis).In the Neurocritical Care unit, patients with primaryneurological diseases such as myasthenia gravis, Guillain-Barrésyndrome, status epilepticus, and stroke have a better outcomethan those patients with secondary neurological diseases. So, wecan conclude that these specialized units have greaterexperience in the anticipation, early recognition, andmanagement of potentially fatal complications.Early identification of patients at risk of life threateningneurological illness in order to manage them properly and toprevent further deterioration is the role of general assessment ofnew patients in a neurological emergency. History taking and arapid neurological assessment of a specific patient in specializedneurocritical care units helps answer the question ‘how sick isthis patient?’.The neurologic screening examination in the emergencysettings focuses primarily on identifying acute, potentially life-threatening processes, and secondarily on identifying disordersthat require other opinions, of other specialists.The importance of urgent neurologic assessment comes fromrecent advances in the management of neurologic disordersneeding timely intervention like thrombolysis in acute ischemic
  15. 15. Assessment of Patients in Neurological Emergency | 15stroke, anticonvulsants for nonconvulsive and subtle generalizedstatus epilepticus, and plasmapheresis for Guillain-Barré, etc.It is obvious that interventions can be time-sensitive and cansignificantly reduce morbidity and mortality.A comprehensive neurologic screening assessment can beaccomplished within minutes if performed in an organized andsystematic manner (Goldberg 1987). Neurologic screeningassessment includes six major components of the neurologicexam, namely:1) Mental status2) Cranial nerve exam3) Motor exam4) Reflexes5) Sensory exam6) Evaluation of coordination and balance.Based on the chief findings of the screening assessment,further evaluation or investigations can be then decided upon.HistoryA careful history is the first step to successful diagnosis, andthen intervention. Careful history provides clues to thepathology of the patient’s condition, and may help direct thediagnostic workup. For example, an alert patient with aheadache associated with neck pain that started after a caraccident might help direct the examination and radiographicimaging to focus on cervical spine injury or neck vessels (carotidor vertebral artery) dissection, while the same patient not in acar accident may direct your attention to a spontaneoussubarachnoid hemorrhage.The history begins with a definition of the patient’s complaint,but aiming at determining key points: time and mode of onset,mode of progression, associated symptoms, and a prior historyof similar conditions. Dramatic or acute onset of neurologicevents suggests a vascular insult and mandates immediateattention and intervention.
  16. 16. 16 | Critical Care in NeurologyPhysical Exam1. Mental statusUsually we start neurologic examination by assessing thepatient’s mental status (Strub 2000).A full mental status exam is not necessary in the patient who isconscious, awake, oriented, and conversant; on the contrary itmust be fully investigated in patients with altered mental status.Sometimes, we can find no change in mental status; at thatpoint careful consideration should be given to concerns offamily.A systematic approach to the assessment of mental status ishelpful in detecting acute as well as any chronic disease, such asdelirious state in a demented patient (Lewis 1995). The CAM(confusion assessment method) score was developed to assist indiagnosing delirium in different contexts. CAM assesses fourcomponents: acute onset, inattention, disorganized thinking oran altered level of consciousness with a fluctuating course. A‘Mini-Mental Status’ test can also be used but usually is reservedfor patients with suspected cognitive dysfunction as it evaluatesfive domains – orientation, registration, attention, recall, andlanguage (Strub 2000).2. Cranial nerve (CN) examCranial Nerves II - VIII function testing are of utmost value in theneurologic assessment in an emergency setting (Monkhouse2006).Cranial Nerves II – Optic nerve assessment involves visualacuity and fields, along with a fundus exam and a swingingflashlight test. Visual field exam using the confrontation methodis rapid and reliable. Visual loss in one eye suggests a nervelesion, i.e., in front of the chiasm; bitemporal hemianopsiasuggests a lesion at the optic chiasm; a quadrant deficit suggestsa lesion in the optic tracts; bilateral visual loss suggests corticaldisease.
  17. 17. Assessment of Patients in Neurological Emergency | 17Assessment of the optic disc, retinal arteries, and retinal veinscan be done by a fundus exam, to discover papilledema, flamehemorrhages or sheathing.Cranial Nerves III, IV, VI – CN III innervates the extraocularmuscles for primarily adduction and vertical gaze. CN IIIfunction is tested in conjunction with IV, which aids in internaldepression via the superior oblique, and VI, which controlsabduction via the lateral rectus. Extraocular muscle function istested for diplopia, which requires binocular vision and thus willresolve when one eye is occluded. Marked nystagmus on lateralgaze or any nystagmus on vertical gaze is abnormal; verticalnystagmus is seen in brainstem lesions or intoxication, whilependular nystagmus is generally a congenital condition.The pupillary light reflex is mediated via the parasympatheticnerve fibers running on the outside of CN III. In the swingingflashlight test a light is shone from one eye to the other; whenthe light is shone directly into a normal eye, both eyes constrictvia the direct and the consensual light response.Pupillary size must be documented. Asymmetry in pupils of lessthan 1 mm is not significant. Significant difference in pupil sizesuggests nerve compression due to aneurysms or due to cerebralherniation, in patients with altered mental status.Bilateral pupillary dilation is seen with prolonged anoxia ordue to drugs (anticholinergics), while bilateral pupillaryconstriction is seen with pontine hemorrhage or as the result ofdrugs (e.g., opiates, clonidine).Cranial Nerve V – Individual branch testing of the trigeminalnerve is unnecessary, as central nervous system lesions affectingCN V usually involve all three branches.Cranial Nerve VII – The facial nerve innervates motorfunction to the face, and sensory function to the ear canal, aswell as to the anterior two-thirds of the tongue. Central lesionscause contralateral weakness of the face muscles below the eyes.Cranial Nerve VIII – The acoustic nerve has a vestibular and acochlear component. An easy screening test for hearing defectsis accomplished by speaking in graded volumes to the patient.
  18. 18. 18 | Critical Care in NeurologyWhen vestibular nerve defects are suspected, patients areassessed for nystagmus, via a past-pointing test and a positiveresponse to the Nylen-Barany maneuver.3. Motor examMotor system assessment focuses on detecting asymmetricstrength deficits, which may indicate an acute CNS lesion.Testing motor power can be difficult or impossible in theuncooperative patient. It is not mandatory to test differentmuscle groups but instead just test for the presence of a “drift”.In diseased patients, the hand and arm on the affected side willslowly drift or pronate when they try to hold their arm outhorizontally, palms up with eyes closed.4. ReflexesFor rapid assessment of reflexes, major deep tendon reflexes andthe plantar reflex must be elicited. Major deep tendon reflexesinclude the patellar reflex, the Achilles reflex, the biceps reflex,and the triceps reflex. Response can be graded from 0 (no reflex)to 4+ (hyperreflexia). Asymmetrical reflexes are the mostimportant as they are considered pathologic. Many reflexesindicate upper motor neuron disease; the most commonlyelicited is Babinski’s reflex.5. Sensory examFor rapid assessment of the sensory system, pain and light touchsensations should be done. Testing for other sensory modalitiesis reserved for patients with suspected neuropathies or forfurther evaluation of sensory complaints.6. Coordination and balanceCoordination depends on functional integration of thecerebellum and sensory input from vision, proprioception, andthe vestibular sense. Coordination assessment is an importantpart of neurological assessment, as many central lesions maypresent only with coordination disturbance, such as cerebellarinfarction, hemorrhage or cerebellar connections insult.
  19. 19. Assessment of Patients in Neurological Emergency | 19By the end of the examination, you should reach a clinicaldiagnosis, which includes answers to the two critical questions,what is the lesion? and where is the lesion?7. Neuroanatomical localizationSome knowledge of neuroanatomy is essential for correctlocalization. The first step in localizing neurological lesionsshould be to determine if it is a central (upper motor neuron)lesion (i.e., in the brain or spinal cord) versus a peripheral (lowermotor neuron) lesion (i.e., nerve or muscle).The hallmark of upper motor neuron lesions is hyperreflexiawith or without increased muscle tone. Central (upper motorneuron) lesions are localized to:Brain– Cortical brain (frontal, temporal, parietal, or occipital lobes)– Subcortical brain structures (corona radiata, internalcapsule, basal ganglia, or thalamus)– Brainstem (medulla, pons, or midbrain)– CerebellumSpinal cord– Cervicomedullary junction– Cervical– Thoracic– Upper lumbarThe hallmark of a lower motor neuron (LMN) lesion isdecreased muscle tone, leading to flaccidity and hyporeflexia.Peripheral LMN lesions are localized to:– Anterior horn cells– Nerve root(s)– Plexus– Peripheral nerve– Neuromuscular junction– Muscle
  20. 20. 20 | Critical Care in NeurologyConclusions1. The neurological screening examination provides theclinician with the necessary data to make managementdecisions.2. A cranial nerve examination gives plenty of data in theemergency setting and is a critical component of thescreening exam.
  21. 21. How to Approach an Unconscious Patient | 212. How to Approach an UnconsciousPatientMagdy Khalaf, Nabil KitchenerComa (from the Greek κώμα [ko̞ma], meaning deep sleep) is astate of unconsciousness lasting more than 6 hours, in which aperson cannot be awakened, fails to respond normally to painfulstimuli, light or sound, lacks a normal sleep-wake cycle and doesnot initiate voluntary actions.All unconscious patients should have neurologicalexaminations to help determine the site and nature of the lesion,to monitor progress, and to determine prognosis. Neurologicalexamination is most useful in the well-oxygenated,normotensive, normoglycemic patient with no sedation, sincehypoxia, hypotension, hypoglycemia and sedating drugsprofoundly affect the signs elicited. Therefore, immediatetherapeutic intervention is a must to correct aberrations ofhypoxia, hypercarbia and hypoglycemia. Medications recentlytaken that cause unconsciousness or delirium must be identifiedquickly followed by rapid clinical assessment to detect the formof coma either with or without lateralizing signs, with or withoutsigns of meningeal irritation, the pattern of breathing, the sizeand reactivity of pupils and ocular movements, the motor
  22. 22. 22 | Critical Care in Neurologyresponse, the airway clearance, the pattern of breathing andcirculation integrity, etc.Special consideration must be given to neurological causeswhich may lead to unconsciousness like status epilepticus (eitherconvulsive or non-convulsive), locked-in state, persistentvegetative state and lastly brain stem death. Any disturbances ofthermoregulation must be measured.Coma may result from a variety of conditions includingintoxication, metabolic abnormalities, central nervous systemdiseases, acute neurologic injuries such as stroke, hypoxia ortraumatic injuries including head trauma caused by falls orvehicle collisions. Looking for the pathogenesis of coma, twoimportant neurological components must function perfectly thatmaintain consciousness. The first is the gray matter covering theouter layer of the brain and the other is a structure located inthe brainstem called the reticular activating system (RAS orARAS), a more primitive structure that is in close connectionwith the reticular formation (RF), a critical anatomical structureneeded for maintenance of arousal. It is necessary to investigatethe integrity of the bilateral cerebral cortices and the reticularactivating system (RAS), as a rule. Unilateral hemispheric lesionsdo not produce stupor and coma unless they are of a masssufficient to compress either the contralateral hemisphere or thebrain stem (Bateman 2001). Metabolic disorders impairconsciousness by diffuse effects on both the reticular formationand the cerebral cortex. Coma is rarely a permanent statealthough less than 10% of patients survive coma withoutsignificant disability (Bateman 2001); for ICU patients withpersistent coma, the outcome is grim.Maneuvers to be established with an unconscious patientinclude cardiopulmonary resuscitation, laboratoryinvestigations, a radiological examination to recognize brainedema, as well as any skull, cervical, spinal, chest, and multipletraumas. Intracranial pressure and neurophysiologicalmonitoring are important new areas for investigation in theunconscious patient.
  23. 23. How to Approach an Unconscious Patient | 23DiagnosisIn the initial assessment of coma, it is common to judge byspontaneous actions, response to vocal stimuli and response topainful stimuli; this is known as the AVPU (alert, vocal stimuli,painful stimuli, unconscious) scale. The most common scalesused for rapid assessment are:1. The Glasgow Coma Scale (GCS), which aims to record theconscious state of a person, in initial as well as continuingassessment. When a patient is assessed and the resulting score iseither 14 (original scale) or 15 (the more widely used modified orrevised scale), this means ‘normal’; while if a patient is unable tovoluntarily open their eyes, does not have a sleep-wake cycle, isunresponsive in spite of strong sensory (painful) or verbalstimuli and who generally scores between 3 to 8 on the GlasgowComa Scale, (s)he is considered to be in coma.2. Pediatric Glasgow Coma Scale: The Pediatric Glasgow ComaScale (PGCS) is the equivalent of the Glasgow Coma Scale used toassess the mental state of adult patients. As with the GCS, thePGCS comprises three tests: eye, verbal and motor responses.The three values separately as well as their sum are considered(Holmes 2005). The lowest possible PGCS is 3 (deep coma ordeath) whilst the highest is 15 (fully awake and aware) (Holmes2005).Diagnosis of coma is simple; but determining the cause of theunderlying pathology may prove to be challenging. As in thosewith deep unconsciousness, there is a risk of asphyxiation ascontrol over the muscles in the face and throat is diminished, sothose in a coma are typically assessed for airway management,nasopharyngeal airway or endotracheal intubation to safeguardthe airway (Formisano 2004).Following the previous assessment patients with impairedconsciousness can be classified according to their degree ofconsciousness disturbance into lethargic, stuporous or comatose.Lethargy resembles sleepiness, except that the patient isincapable of becoming fully alert; these patients are conversant
  24. 24. 24 | Critical Care in Neurologyand attentive but slow to respond, unable to adequately performsimple concentration tasks such as counting from 20 to 1, orreciting the months in reverse.Stupor means incomplete arousal to painful stimuli, little or noresponse to verbal commands, the patient may obey commandstemporarily when aroused by noxious stimuli but more oftenonly by pain.Coma is the absence of verbal or complex motor responses toany stimulus (Stevens 2006).Basic assessments1. Pupillary functions may be normal if the lesion is rostral tothe midbrain, while if the injury is diffuse, e.g., global cerebralanoxia or ischemia, the pupillary abnormality is bilateral. Pupilsize is important as midposition (2-5 mm) fixed or irregularpupils imply a focal midbrain lesion; pinpoint reactive pupilsoccur in global hypoxic ischemic insult with pontine damage, orpoisoning with opiates and cholinergic active materials; andbilateral fixed and dilated pupils can reflect central herniationor global hypoxic ischemic or poisoning with barbiturates,scopolamine, and atropine. Unilateral dilated pupil suggestscompression of the third cranial nerve and midbrain, whichnecessitates an immediate search for a potentially correctableabnormality to avoid irreversible injury. In case of post-cardiacarrest coma, if pupils remain nonreactive for more than 6-8hours after resuscitation, the prognosis for neurologicalrecovery is generally guarded (Stevens 2006).2. Posturing of the body: decorticate posturing (painful stimuliprovoke abnormal flexion of upper limbs) indicates a lesion atthe thalamus or cortical damage; decerebrate posturing (thearms and legs extend and pronate in response to pain) denotesthat the injury is localized to the midbrain and upper pons; aninjury of the lower brain stem (medulla) leads to flaccidextremities.
  25. 25. How to Approach an Unconscious Patient | 253. Ocular reflexes: assessment of the brainstem and corticalfunctions happen through special reflex tests such as theoculocephalic reflex test (Doll’s eyes test), oculovestibular reflextest (cold caloric test), nasal tickle, corneal reflex, and the gagreflex.4. Vital signs: temperature (rectal is most accurate), bloodpressure, heart rate (pulse), respiratory rate, and oxygensaturation (Inouye 2006). It is mandatory to evaluate these basicvital signs quickly and efficiently to gain insight into a patient’smetabolism, fluid status, heart function, vascular integrity, andtissue oxygenation status.5. The respiratory pattern (breathing rhythm) is significant andshould be noted in a comatose patient. Certain stereotypicalpatterns of breathing have been identified including Cheyne-Stokes respiratory pattern, where the patient’s breathing isdescribed as alternating episodes of hyperventilation and apnea,a dangerous pattern often seen in pending herniation, extensivecortical lesions, or brainstem damage. Apneustic breathing ischaracterized by sudden pauses of inspiration and is due topontine lesion. Ataxic (Biot’s) breathing is an irregular chaoticpattern and is due to a lesion of the medulla. The first priority inmanaging a comatose patient is to stabilize the vital functions,following the ABC rule (Airway, Breathing, and Circulation).Once a person in a coma is stable, assessment of the underlyingcause must be done, including imaging (CT scan, CTangiography, magnetic resonance imaging (MRI), magneticresonance angiography (MRA) and magnetic resonancevenography (MRV) if needed ) and special studies, e.g., EEG andtranscranial Doppler.Coma is a medical emergency, and attention must first bedirected to maintaining the patient’s respiration and circulationas previously mentioned using intubation and ventilation,administration of intravenous fluids or blood and othersupportive care as needed. Measurement of electrolytes is acommonly performed diagnostic procedure, most often sodium
  26. 26. 26 | Critical Care in Neurologyand potassium; chloride levels are rarely measured except forarterial blood gases (Bateman 2001). Once a patient is stable andno longer in immediate danger, the medical staff should startparallel work, first investigating the patient to find out anyunderlying pathology of his presenting illness, second, managingthe presenting illness symptoms. Infections must be preventedand a balanced nutrition provided. The nursing staff, to guardagainst pressure ulcers, may move the patient every 2–3 hoursfrom side to side and, depending on the state of consciousness,sometimes to a chair. Physical therapy may also be used toprevent contractures and orthopedic deformities that wouldlimit recovery for those patients who emerge from coma(Wijdicks 2002).People may emerge from a coma with a combination ofphysical, intellectual and psychological difficulties that needspecial attention; recovery usually occurs gradually and somepatients acquire more and more ability to respond, others neverprogress beyond very basic responses. Regaining consciousnessis not instant in all comatose patients: in the first days, patientsare only awake for a few minutes, the duration of awake timegradually increases, until they regain full consciousness. Thecoma patient awakens sometimes in a profound state ofconfusion, not knowing how they got there and sometimessuffering from dysarthria, the inability to articulate speech, andother disabilities. Time is the best general predictor of a chanceof recovery: after 4 months of coma caused by brain damage, thechance of partial recovery is less than 15%, and the chance of fullrecovery is very low (Wijdicks 2002). Coma which lasts secondsto minutes may result in post-traumatic amnesia (PTA) lastingfrom hours to days; recovery occurs over days to weeks. Comawhich lasts hours to days may result in PTA lasting from days toweeks; its recovery occurs over months. Coma which lasts weeksmay result in PTA that lasts months; recovery occurs overmonths.
  27. 27. How to Approach an Unconscious Patient | 27General Care of the Comatose Patient1. Airway protection: adequate oxygenation, ventilation andprevention of aspiration are the most important goals; mostpatients will require endotracheal intubation and frequentorotracheal suctioning.2. Intravenous hydration: stuporous patients should receivenothing by mouth; use only isotonic fluids in these patients toavoid increasing the size of the cerebral edema or increasedintracranial pressure (ICP).3. Nutrition: enteral feeds via a small bore nasogastric tube.4. Skin: the patient must be turned every 1-2 hours to preventpressure sores; an inflatable or foam mattress and protectiveheel pads may also be beneficial.5. Eyes: prevent corneal abrasion by taping the eyelids shut orby applying a lubricant.6. Bowel care: constipation and gastric stress ulcers should beavoided.7. Bladder care: indwelling urinary catheters are a commonsource of infection and should be used judiciously; intermittentcatheterization every 6 hours when possible.8. Joint mobility: passive range of motion daily exercises toprevent contractures.9. Deep venous thrombosis prophylaxis: subcutaneousanticoagulants and external pneumatic compression stockings orboth (Upchurch 1995).To complete this important critical situation, we will discusstwo other categories, the permanent vegetative state and locked-in syndrome.Permanent Vegetative StatePermanent vegetative state (PVS) means an irreversible state ofwakefulness without awareness, associated with sleep-wakecycles and preserved brainstem functions. There are no reliable
  28. 28. 28 | Critical Care in Neurologyset of criteria defining and ensuring diagnosis of PVS in infantsunder 3 months old, apart from anencephalics.There are three major categories of disease in adults andchildren that result in PVS, upon which the outcome of PVSdepends:A. In acute traumatic and nontraumatic brain injury, PVSusually evolves within 1 month of injury from a state of eyes-closed coma to a state of wakefulness without awareness withsleep-wake cycles and preserved brainstem functions.B. Some degenerative and metabolic disorders of the brain (i.e.,late stage of dementia of Alzheimer type, end stage of Parkinsondisease, and motor neuron disease, pontine myelinolysis, severeuncorrected hypoglycaemic coma) inevitably progress toward anirreversible vegetative state. Patients who are severely impairedbut retain some degree of awareness may lapse briefly into avegetative state from the effects of medication, infection,superimposed illnesses, or decreased fluid and nutritionalintake. Such a temporary encephalopathy must be correctedbefore labeling that patient with the diagnosis of PVS.Consciousness recovery is unlikely if the vegetative state persistsfor several months.C. The third cause is severe developmental malformations ofthe nervous system - the developmental vegetative state is aform of PVS that affects some infants and children with severecongenital malformations of the nervous system. These childrendo not acquire awareness of self or their environment. Thisdiagnosis can be made at birth only in infants with anencephaly.For children with other severe malformations who appearvegetative at birth, observation for 3 to 6 months isrecommended to determine whether these infants acquireawareness. The majority of such infants who are vegetative atbirth remain vegetative; those who acquire awareness usuallyrecover only to a severe disability.
  29. 29. How to Approach an Unconscious Patient | 29DiagnosisThe vegetative state is diagnosed, according to its definition, asbeing persistent at least for one month. Based upon class IIevidence and consensus that reflects a high degree of clinicalcertainty, the following criteria is standard concerning PVS:– PVS can be judged to be permanent, at 12 months aftertraumatic brain injury in adults and children. Specialattention to signs of awareness should be devoted tochildren during the first year after traumatic injury.– PVS can be judged to be permanent if it lasts more than 3months, in case of nontraumatic brain injury in both adultsand children.– The chance for recovery, after these periods, is exceedinglylow and recovery is almost always to a severe disability.ManagementWhen a patient has been diagnosed as being in a PVS by aphysician skilled in neurological assessment and diagnosis,physicians have the responsibility of discussing with the familyor surrogates the probability of the patient’s attaining thevarious stages of recovery or remaining in a PVS:– Patients in PVS should receive appropriate medical, nursing,or home care to maintain their personal dignity andhygiene.– Physicians and the family/surrogates must determineappropriate levels of treatment relative to theadministration or withdrawal of 1) medications and othercommonly ordered treatments; 2) supplemental oxygen anduse of antibiotics; 3) complex organ-sustaining treatmentssuch as dialysis; 4) administration of blood products; and 5)artificial hydration and nutrition.Recovery from PVS can be defined in terms of recovery ofconsciousness and function. Recovery of consciousness can beconfirmed when a patient shows reliable signs of awareness of
  30. 30. 30 | Critical Care in Neurologyself and their environment, reproducible voluntary behavioralresponses to visual and auditory stimuli, and interaction withothers. Recovery of function occurs when a patient becomesmobile and is able to communicate, learn, and perform adaptiveskills and self care and participate in recreational or vocationalactivities. Using these parameters, recovery of function can bedefined with the Glasgow Outcome Scale.The life span of adults and children in a PVS proves to bereduced; for most PVS patients, life expectancy ranges from 2 to5 years and survival beyond 10 years is unusual. Once PVS isconsidered permanent, a “Do not resuscitate (DNR)” order isappropriate which includes no ventilatory or cardiopulmonaryresuscitation. The decision to implement a DNR order, however,may be made earlier in the course of the patient’s illness if thereis an advanced directive or agreement by the appropriatesurrogate of the patient and the physicians responsible for thecare of the patient (Plum 2007).Locked-in SyndromeLocked-in syndrome usually results in quadriparesis and theinability to speak in otherwise cognitively intact individuals.Patients with locked-in syndrome may be able to communicatewith others through coded messages by blinking or moving theireyes, which are often not affected by the paralysis. Patients withlocked-in syndrome are conscious and aware with no loss ofcognitive functions. They sometimes can retain proprioceptionand sensation throughout their body. Some patients with locked-in syndrome may have the ability to move some muscles of theface, and some or all of the extraocular eye muscles. Patientswith locked-in syndrome lack coordination between breathingand voice that restricts them from producing voluntary sounds,even though the vocal cords themselves are not paralyzed. Inchildren, the commonest cause is a stroke of the ventral pons.Unlike persistent vegetative state, locked-in syndrome is causedby damage of the lower brain and brainstem without damage to
  31. 31. How to Approach an Unconscious Patient | 31the upper brain (Leon Carrion 2002). Possible causes of locked-insyndrome include: traumatic brain injury, diseases of thecirculatory system, overdose of certain drugs, various causeswhich lead to damage to the nerve cells, particularly destructionof the myelin sheath, e.g., central pontine myelinolysissecondary to rapid correction of hyponatremia and basilarartery (ischemic or hemorrhagic) stroke.There is neither a standard treatment for locked-in syndrome,nor is there a cure, but stimulation of muscle reflexes withelectrodes (NMES) has been known to help patients regain somemuscle function. Assistive computer interface technologies incombination with eye tracking may be used to help patientscommunicate. Direct brain stimulation research developed atechnique that allows locked-in patients to communicate viasniffing (Leon Carrion 2002). It is extremely rare for anysignificant motor function to return and the majority of locked-in syndrome patients do not regain motor control, but devicesare available to help patients communicate. 90% die within thefirst four months after onset. However, some patients continueto live for much longer periods of time (Bateman 2001).Brain DeathAfter exclusion of the previous syndromes, and in the absenceof brain stem reflexes, brain death in deeply comatose patientsshould be established through the following criteria:1. Irreversible coma2. Absence of brain stem reflexes3. Absence of spontaneous respiration (Wood 2004)
  32. 32. 32 | Critical Care in Neurology3. Documentation and ScoresNabil KitchenerMedical documentation is important for communication amonghealth care professionals, for research, legal defense, andreimbursement. Neurological scoring systems are used to assessthe severity of illness in patients with neurological emergencies,and can be used to monitor the clinical course, to documentcomplications of therapy and to help identify prognostic factors.Two types of scoring systems are commonly used: neurologicalscoring systems, to quantify neurological deficits, like theGlasgow Coma Scale or the Mini-Mental Status Examination; andfunctional scoring systems to characterize patients’ abilities toperform activities of daily living, used to quantify the functionaloutcome with or without therapy, like the Canadian NeurologicalScore, the NIH stroke scale, the modified Rankin scale, theexpanded disability status scale, the Richmond agitationsedation score and the confusion assessment method.Neurological scoring is used in the critical care unit while scoresfor activities of daily living are used for the outcome assessment.Intensive care units (ICUs) provide a service for patients withpotentially recoverable diseases who can benefit from moredetailed observation and treatment than is usually available onthe general wards. Patients may be discharged from the ICUwhen their physiologic status has stabilized and the need for ICU
  33. 33. Documentation and Scores | 33monitoring and care is no longer necessary (Egol 1999).However, a number of patients who are successfully dischargedfrom intensive care subsequently die during their hospitaladmissions. This may indicate premature discharge from the ICUor suboptimal management in the ICU or the general ward(Campbell 2008). As trends move towards earlier ICU discharge,it becomes increasingly important to be able to identify thosepatients at high risk of subsequent clinical deterioration, whomight benefit from longer ICU stays or from transfers tointermediate care units. A strategy to reduce prematuredischarges in patients at high risk of in-hospital death couldresult in a 39% reduction in post-ICU death in these patients(Daly 2001). It can be concluded that reliable baseline and follow-up assessment is crucial to document any improvement ordeterioration in neurological status of patients admitted to aneurocritical care unit. Interrater differences may be significant,so the need for standardized neurological scales and scorescomes into play.Scales seek to quantify different aspects of function within theframework of the World Health Organization hierarchy ofimpairment, disability, and handicap (Thuriaux 1995). Since theintroduction of the Mathew scale in 1972 (Mathew 1972), therehas been a steadily increasing number of scales that seek toquantify neurological impairment. These scales involve scoringdifferent modalities of neurological function and then sum thescores to provide an index for neurological status. These scaleswere developed for a variety of reasons, including monitoringneurological status for improvement or deterioration (Cote 1986)and predicting final outcome in a defined group of patients(Brott 1989). The primary purpose for these scales inneurocritical care units is to compare the baseline neurologicalimpairment severity of patients at admission, and to quantifyneurological recovery over time, to avoid premature dischargefrom the neurocritical care unit and promote early detection ofdeterioration and prompt management.
  34. 34. 34 | Critical Care in NeurologyScoring and DocumentationEach neurocritical care unit should adopt a special scoring anddocumentation system, to be used to assess and documentbaseline patient neurological status and status at time ofdischarge. These include:– Vital Signs: BP, temp, pulse, respiration, oximetry– Pupils: size and reaction to light– Eye movement: gaze, vergence, individual extraocularmovement and nystagmus– Mental status: LOC, orientation and speech– Motor functions: state, power, tone, deep reflexes andpathological reflexes– Coordination: gate, upper and lower limbs, if applicableThere are many scales used to assess these functions; eachcritical care unit can adopt a set that can be used by its staff.Tables 3.1, 3.2, and 3.3 show some of the commonly used scalesin clinical practice.
  35. 35. Documentation and Scores | 35Table 3.1 – Neurological Scales used for assessment of level ofconsciousness and mental statusName and Source Strengths and WeaknessesLevel-of-consciousness scaleGlasgow Coma Scale(Teasdale 1974, 1979)Strength: Simple, valid, reliable, for assessment oflevel-of-consciousness.Weaknesses: none observed.Full OutlineUnresponsiveness – FOURScore(Wijdicks 2005)Strength: The FOUR score is easy to apply andprovides more neurological details than theGlasgow scale. This scale is able to detectconditions such locked-in syndrome and thevegetative state, which are not detected by theGCS.Weaknesses: none observed.Delirium ScaleConfusion AssessmentMethod (CAM)(Inouye 1990)Strength: CAM-ICU is an adaptation of theConfusion Assessment Method (CAM), which wasadapted to be a delirium assessment tool for use inICU patients (e.g., critically ill patients on and offthe ventilator who are largely unable to talk).Weaknesses: none observed.Richmond AgitationSedation Scale (RASS)(Sessler 2002)Strength: RASS is logical, easy to administer, andreadily recalled. RASS has high reliability andvalidity in medical and surgical, ventilated andnon-ventilated, and sedated and non-sedatedadult ICU patients.Weaknesses: none observedMental status screeningFolstein Mini-Mental StateExamination (Folstein 1975)Strength: Widely used for screening.Weaknesses: Several functions with summedscore. May mis-classify patients with aphasia.Neurobehavioral CognitionStatus Exam (NCSE)(Kiernan 1987)Strength: Predicts gain in Barthel Index scores.Unrelated to age.Weaknesses: Does not distinguish right from lefthemisphere. No reliability studies in stroke. Nostudies of factorial structure. Correlates witheducation.
  36. 36. 36 | Critical Care in NeurologyTable 3.2 – Neurological Scales used for assessment of stroke deficitsName and Source Strengths WeaknessesMeasures of disability/activities of daily living (ADL)Barthel Index(Mahoney 1965,Wade 1988)Widely used for stroke.Excellent validity andreliability.Low sensitivity for high-levelfunctioningFunctionalIndependenceMeasure (FIM)(Granger 1987)Widely used for stroke.Measures mobility, ADL,cognition, functionalcommunication."Ceiling" and "floor" effectsStroke deficit scalesNIH Stroke Scale(Brott 1989)Brief, reliable, can beadministered by non-neurologistsLow sensitivityCanadianNeurological Scale(Cote 1986)Brief, valid, reliable Some useful measures omittedAssessment of motor functionFugl-Meyer(Fugl-Meyer 1975)Extensively evaluatedmeasure. Good validityand reliability forassessing sensorimotorfunction and balanceConsidered too complex and time-consuming by manyMotor AssessmentScale (Poole 1988)Good, brief assessment ofmovement and physicalmobilityReliability assessed only in stablepatients. Sensitivity not testedMotricity Index(Collin 1990)Brief assessment of motorfunction of arm, leg, andtrunkSensitivity not testedBalance assessmentBerg BalanceAssessment(Berg 1992)Simple, well establishedwith stroke patients,sensitive to changeNone observedMobility assessmentRivermeadMobility Index(Collen 1991)Valid, brief, reliable test ofphysical mobilitySensitivity not tested
  37. 37. Documentation and Scores | 37Name and Source Strengths WeaknessesAssessment of speech and language functionsBoston DiagnosticAphasiaExamination(Goodglass 1983)Widely used,comprehensive, goodstandardization data,sound theoreticalrationaleLong time to administer; half ofpatients cannot be classifiedPorch Index ofCommunicativeAbility (PICA)(Porch 1981)Widely used,comprehensive, carefultest development andstandardizationLong time to administer. Specialtraining required to administer.Inadequate sampling of languageother than one word and singlesentencesWestern aphasiaBattery (Kertesz1982)Widely used,comprehensiveLong time to administer. "Aphasiaquotients" and "taxonomy" ofaphasia not well validatedTable 3.3 – Neurological Scales used for assessment of health status andglobal disabilitiesType Name andSourceStrengths WeaknessesGlobaldisability scaleRankin Scale(Rankin 1957,Bonita 1988,Van Swieten1988)Good for overallassessment ofdisability.Walking is the onlyexplicit assessmentcriterion. LowsensitivityHealth status/quality of lifemeasuresMedicalOutcomes Study(MOS) 36 ItemShort-FormHealth Survey(Ware 1992)Generic health statusscale SF36 is improvedversion of SF20. Brief,can be self -administered oradministered by phoneor interview. Widelyused in the USPossible "floor" effectin seriously ill patients(especially for physicalfunctioning), suggests itshould besupplemented by anADL scale in strokepatientsSickness ImpactProfile (SIP)(Bergner 1981)Comprehensive andwell-evaluated. Broadrange of items reduces"floor" or "ceiling"effectsTime to administersomewhat long.Evaluates behaviorrather than subjectivehealth; needs questionson well-being,happiness, andsatisfaction
  38. 38. 38 | Critical Care in NeurologyDeliriumDelirium is a disturbance of consciousness characterized byacute onset and fluctuating course of inattention accompaniedby either a change in cognition or a perceptual disturbance, sothat a patient’s ability to receive, process, store, and recallinformation is impaired.Delirium, a medical emergency, develops rapidly over a shortperiod of time, is usually reversible, and is a direct consequenceof a medical condition or a brain insult. Many delirious ICUpatients have recently been comatose, indicating a fluctuation ofmental status. Comatose patients often, but not always, progressthrough a period of delirium before recovering to their baselinemental status.ICU delirium is a predictor of increased mortality, length ofstay, time on ventilator, costs, re-intubation, long-term cognitiveimpairment, and discharge to long-term care facility; itnecessitates special attention, assessment and management.Delirium assessment is actually an important part of the overallassessment of consciousness.Delirium includes three subtypes: hyperactive, hypoactive andmixed. Hyperactive delirium is characterized by agitation,restlessness, and attempts to remove tubes and lines. Hypoactivedelirium is characterized by withdrawal, flat affect, apathy,lethargy, and decreased responsiveness. Mixed delirium ischaracterized by fluctuation between the hypoactive andhyperactive. In ICU patients mixed and hypoactive are the mostcommon, and are often undiagnosed if routine monitoring is notimplemented. Few ICU patients (less than 5%) experience purelyhyperactive delirium.The Confusion Assessment Method (CAM) was created in 1990by Sharon Inouye, and was intended to be a bedside assessmenttool usable by non-psychiatrists to assess for delirium (Inouye1990). The CAM-ICU is an adaptation of this tool for use in ICUpatients (e.g., critically ill patients on and off the ventilator whoare largely unable to talk).
  39. 39. Brain Injuries | 394. Brain InjuriesMagdy Khalaf, Nabil KitchenerNeurocritical care focuses on critically ill patients with primaryor secondary neurological problems. Initially neurocritical carewas developed to manage postoperative neurosurgical patients;it then expanded to the management of patients with traumaticbrain injury (TBI), intracranial hemorrhage and complications ofsubarachnoid hemorrhage, including vasospasm, elevatedintracranial pressure (ICP) and the cardiopulmonarycomplications of brain injury (Bamford 1992). The strikingimprovements noted in many studies suggest that high-qualityneurocritical care with the delivery of targeted therapeuticinterventions does have an impact, not only on survival, butimportantly also on the quality of survival.Types of Brain InjuriesPrimary brain injuriesIschemic brain injury: either global, which includes cardiacarrest or anoxia, or regional ischemic brain injury, whichincludes vasospasm, compression of blood vessels or stroke.Stroke can be classified into ischemic and hemorrhagic strokes.Ischemic stroke accounts for 80% of all strokes and can befurther classified into thrombotic or embolic stroke; ischemic
  40. 40. 40 | Critical Care in Neurologythrombotic stroke accounts for 77% while ischemic embolicstroke constitutes the remainder.Hemorrhagic strokes constitute 10-20% of all strokes, and canbe further classified into two types, the intracerebralhemorrhage that constitutes up to 75% and the subarachnoidhemorrhage that makes up the other 25%.Acute ischemic stroke is the third leading cause of death inindustrialized countries and the most frequent cause ofpermanent disability in adults worldwide, so understanding thepathogenesis of ischemic stroke is mandatory. Despite greatstrides in understanding the pathophysiology of cerebralischemia, therapeutic options remain limited. Only recombinanttissue plasminogen activator (rTPA) for thrombolysis iscurrently approved for use in the management of acute ischemicstroke.However, its use is limited by its short therapeutic window (3-4.5 hours), complications from the risk of hemorrhage, and thepotential damage from reperfusion injury. Effective strokemanagement requires recanalization of the occluded bloodvessels. However, reperfusion can cause neurovascular injury,leading to cerebral edema, brain hemorrhage, and neuronaldeath by apoptosis or necrosis (Hajjar 2011).Central nervous system (CNS) infections: Acute onset feverwith altered mental status is a problem commonly encounteredby the physician in the emergency setting. “Acute febrileencephalopathy” is a commonly used term for description of thealtered mental status that either accompanies or follows a shortfebrile illness. CNS infections are the most common cause ofnontraumatic disturbed consciousness. The etiologic agents maybe viruses, bacteria, or parasites. Central nervous systeminfections are classified into categories beginning with those inimmunocompetent hosts followed by infection with the humanimmunodeficiency virus (HIV) and its opportunistic infections.The viruses responsible for most cases of acute encephalitis inimmunocompetent hosts are herpes viruses, arboviruses, andenteroviruses. Neurotropic herpes viruses that cause
  41. 41. Brain Injuries | 41encephalitis predominantly in immunocompetent hosts includeherpes simplex virus 1 (HSV-1) and 2 (HSV-2), human herpesvirus 6 (HHV-6) and 7 (HHV-7), and Epstein-Barr virus (EBV).Cytomegalovirus (CMV) and varicella-zoster virus (VZV) may insome situations cause encephalitis in immunocompetentpatients, but more commonly they produce an opportunisticinfection in immunocompromised individuals, such as thosewith HIV infection, organ transplant recipients, or other patientsusing immunosuppressive drugs. HSV-1 is the most commoncause of severe sporadic viral encephalitis in the United States;diagnosis has been become more familiar due to the availabilityof cerebrospinal fluid (CSF) polymerase chain reaction (PCR)analysis techniques that allow for rapid, specific, and sensitivediagnoses. The use of CSF PCR instead of brain biopsy as thediagnostic standard for HSV encephalitis has expandedawareness of mild or atypical cases of HSV encephalitis. Adultencephalitis is caused by 2 viral serotypes, HSV-1 and HSV-2.Patients with greater than 100 DNA copies/µL HSV in CSF aremore likely than those with fewer copies to have a reduced levelof consciousness, more significant abnormal findings onneuroimaging, a longer duration of illness, higher mortality, andmore sequelae (Domingues 1997). EBV is almost never culturedfrom CSF during infection, and serological testing isinconclusive, so CSF PCR diagnosis is mandatory.Semiquantitative PCR analysis of EBV DNA suggests that copynumbers are significantly higher in patients with active EBVinfection. HHV-6 and -7 can cause exanthema subitum, andappear to be associated with febrile convulsions, even in theabsence of signs of exanthema subitum. Almost all children(>90%) with exanthema subitum have HHV-6 or HHV-7 DNA inCSF. Inflammatory primary brain damage like meningitis andencephalitis come from pyogenic infections that reach theintracranial structures in one of two ways - either byhematogenous spread (infected thrombi or emboli of bacteria) orby extension from cranial structures (ears, paranasal sinuses,osteomyelitic foci in the skull, penetrating cranial injuries or
  42. 42. 42 | Critical Care in Neurologycongenital sinus tracts). In a good number of cases, infection isiatrogenic, being introduced in the course of cerebral or spinalsurgery, during the placement of a ventriculoperitoneal shunt orrarely through a lumbar puncture needle. Nowadays, nosocomialinfections are as frequent as the non-hospital acquired variety.The reason for altered sensorium in meningitis is postulated tobe the spillage of inflammatory cells to the adjacent brainparenchyma and the resultant brain edema (Levin 1998).Compressive brain injury: e.g., tumors and cerebral brainedema are considered as important causes for impairment of thelevel of consciousness. During tumor growth, cerebral tissuesadjacent to the tumor and nearby venules are compressed,which results in elevation of capillary pressure, particularly inthe cerebral white matter, and there is a change in cerebralblood flow and consequently intracranial pressure. At that stagethe tumor begins to displace tissue, which eventually leads todisplacement of tissue at a distance from the tumor, resulting infalse localizing signs such as transtentorial herniations,paradoxical corticospinal signs of Kernohan and Woltman, thirdand sixth nerve palsies and secondary hydrocephalus, originallydescribed in tumor patients.Secondary brain injuriesSecondary brain injuries include renal coma, hepatic coma, saltand water imbalance, disturbance of glucose metabolism, otherendocrinal causes of coma, disturbances of calcium andmagnesium metabolism, drug intoxication and other materialintoxication, not only drug toxicity, hypertensive and metabolicencephalopathies, sleep apnea syndromes and other ventilatordisturbances. Mechanisms of secondary brain injury includehypoxia, hypoperfusion, reperfusion injury with free radicalformations, release of excitatory amino acids and harmfulmediators from injured cells, electrolyte and acid base changesfrom systemic or regional ischemia (Semplicini 2003).The primary goal in managing neurologically compromisedpatients includes (Stasiukyniene 2009) stabilizing the brain
  43. 43. Brain Injuries | 43through the maintenance of oxygen delivery via the followingparameters:1. Assuring systemic oxygen transport and adequateoxygenation, maintaining hemoglobin level (atapproximately 10 g/dl or more) and cardiac output.2. Assuring optimal mean arterial pressure (MAP). Manyinsults are associated with hypertension, which may be aphysiologic compensation, so excessive lowering of bloodpressure may induce secondary ischemia. In general,systolic pressure should be treated when more than 200mmHg or MAP when more than 125 mmHg. Cautiousreduction in mean arterial pressure by only 25% isrecommended (Adams 2007).3. Avoiding prophylactic or routine hyperventilation - adecrease in extracellular brain pH may producevasoconstriction in responsive vessels and reduce CBF toalready ischemic zones. This applies to patients with headtrauma in whom routine hyperventilation is no longerconsidered desirable; brief hyperventilation may belifesaving in the patient with herniation, pending theinstitution of other methods to lower elevated ICP.4. Assuring euvolemia. Hypervolemia may also be helpfulwhen vasoconstriction is suspected, as in the setting ofsubarachnoid hemorrhage.5. Consideration should be given to administeringintravenous lidocaine 1.5 mg/kg or intravenous thiopental(5 mg/kg) to blunt the rise in ICP associated withintubation.6. Nimodipine should be instituted immediately in patientswith SAH and is advocated by some in patients withsubarachnoid bleeding after head trauma. Nimodipineprobably improves outcome by decreasing calcium-mediated neuronal toxicity.7. Using normal saline as the primary maintenance fluid;dextrose administration is usually avoided unless the
  44. 44. 44 | Critical Care in Neurologypatient is hypoglycemic; hypotonic solutions should also beavoided.8. Assessing and treating coagulation defects.9. Sedation and/or neuromuscular blockade after intubationmay be required to control harmful agitation.10. If seizure occurrs, it should be aggressively treated.11. Titration of the ICP and cerebral perfusion pressure.Management of Special IssuesTraumatic brain injuryOutcome after traumatic brain injury depends upon the initialseverity of the injury, age, the extent of any subsequentcomplications, and how these are managed. Much of the earlymanagement of traumatic brain injury falls upon emergencyroom staff, primary care and ambulance services prior tohospital admission. Most patients who attend hospital after atraumatic brain injury do not develop life-threateningcomplications in the acute stage. However, in a small butimportant subgroup, the outcome is made worse by failure todetect promptly and deal adequately with complications.General rules:1. A traumatic brain injury should be discussed withneurosurgery whena. a CT scan in a general hospital shows a recentintracranial lesionb. a patient fulfills the criteria for CT scanning but thiscannot be done within an appropriate periodc. whatever the result of the CT scan, the patient hasclinical features that suggest that specialistneurological assessment, monitoring, or managementare appropriate. Reasons include:i. Persistent coma (GCS <9, no eye opening) afterinitial resuscitationii. Confusion persisting for more than 4 hours
  45. 45. Brain Injuries | 45iii. Deterioration in level of consciousness afteradmission (a sustained decrease of one point in themotor or verbal GCS subscores, or 2 points on theeye opening subscale of the GCS)iv. Persistent focal neurological signsv. A seizure without full recoveryvi. Compound depressed fracturevii. Suspected or definite penetrating injuryviii.A CSF leak or other sign of base of skull fracture2. Keep sodium >140 mmol/L. A fall in serum sodium producesan osmotic gradient across the blood–brain barrier, andaggravates cerebral edema.3. Avoid hyperglycemia (treat blood glucose >11 mmol/L).Hyperglycemia increases cerebral lactic acidosis, whichmay aggravate ischemic brain injury.4. Feed via an orogastric tube. Gastric motility agents can begiven as required.5. Use TED stockings; avoid low-dose heparin.6. Apply 15–30° head-up tilt with head kept in neutralposition; this may improve CPP.7. No parenteral hypotonic fluid must be given.Acute strokeThe World Stroke Organization declared a public healthemergency on World Stroke Day (WSO 2010). There are 15million people who have a stroke each year. According to theWorld Health Organization, stroke is the second leading cause ofdeath for people above the age of 60, and the fifth leading causein people aged 15 to 59. Stroke also happens to children,including newborns. Each year, nearly six million people diefrom stroke. In fact, stroke is responsible for more deathsannually than those attributed to AIDS, tuberculosis and malariaput together. Stroke is also the leading cause of long-termdisability irrespective of age, gender, ethnicity or country.Yet for many healthcare staff it remains an area of therapeuticnihilism and thus uninteresting and neglected (WSO 2010). This
  46. 46. 46 | Critical Care in Neurologynegative perception is shared by the general public, who oftenhas a poor understanding of the early symptoms and significanceof a stroke.Yet within the last few years there have been many importantdevelopments in the approach to awareness and caring forstroke patients, for both the acute management and secondaryprevention. Clinical research and interest in stroke has increasedgreatly in the last few years. Each minute of brain ischemiacauses the destruction of 1.9 million neurons, 14 billionsynapses, and 7.5 miles of myelinated nerves (Hand 2006).Ischemic stroke is characterized by one or more focalneurological deficits corresponding to the ischemic brainregions. It requires an immediate decision regardingthrombolytic therapy (tissue plasminogen activator, TPA, in thedosage of 0.9 mg/kg, 10% as a bolus over 1 minute and infuse theremaining 90% over the next hour).Wise control of hypertension is essential, control ofhyperglycemia and fever is protective against more destructionof neurons (Mistri 2006).Status epilepticus (SE)Status epilepticus is defined as more than 30 minutes ofcontinuous seizure activity or recurrent seizure activity withoutan intervening period of consciousness (Manno 2003).In one survey, only 10% of patients who develop seizures in amedical ICU will develop SE. The most common causes of SE arenoncompliance with or withdrawal of antiepileptic medications,cerebrovascular disease and alcohol withdrawal.The hypersynchronous neuronal discharge that characterizes aseizure is mediated by an imbalance between excitation andinhibition. The adverse effects of generalized seizures includehypertension, lactic acidosis, hyperthermia, respiratorycompromise, pulmonary aspiration or edema, rhabdomyolysis,self-injury and irreversible neurological damage (Bassin 2002).The most common and potentially dangerous forms of statusepilepticus are generalized convulsive status epilepticus, non-
  47. 47. Brain Injuries | 47convulsive generalized status epilepticus, refractory statusepilepticus and myoclonic status epilepticus. Also, seizures thatpersist for longer than 5-10 minutes should be treated urgentlybecause of the risk of permanent neurological injury andbecause seizures become refractory to therapy the longer theypersist (Stasiukyniene 2009).General measures for management are shown in Table 4.1.Intravenous drug therapy for convulsive seizures in the ICU areas follows:1. Lorazepam: 0.10 mg/kg up to 2 mg/min or diazepam 0.15mg/kg; if seizure continues, give2. Fosphenytoin: 20 mg/kg up to 150 mg/min or phenytoin 20mg/kg up to 50 mg/min; if seizure continues, one of thefollowing medications may be used but these require intubationand mechanical ventilation:– phenobarbital 20 mg/kg up to 50 mg/min– propofol 3-5 mg/kg load then 1-15 mg/kg/hr– midazolam 0.2 mg/kg load then 0.05-2 mg/kg/hr– pentobarbital 5-15 mg/kg load, then 0.5-10 mg/kg/hrNeuromuscular emergenciesNeuromuscular emergencies are composed of a group of severelife-threatening neuromuscular diseases such as myastheniccrises, cholinergic crises, critical illness myopathy and criticalillness polyneuropathy.Respiratory paralysis occurs in a small percentage of patientswith acute neuromuscular disease and accounts for less than 1%of admissions to general intensive care units. Its developmentmay be insidious so that patients with acute neuromusculardisease should have their vital capacity monitored. Orotrachealintubation and ventilatory support should be institutedprophylactically when vital capacity is falling towards 15 ml/kg.Earlier intervention is necessary in the presence of bulbar palsy.
  48. 48. 48 | Critical Care in NeurologyTable 4.1 – General measures for management of Status Epilepticus*1 (0–10 minutes)Assess cardiorespiratory functionSecure airway and resuscitateAdminister oxygen2 (0–60 minutes)Institute regular monitoringEmergency antiepileptic drug therapySet up intravenous linesEmergency investigationsAdminister glucose (50 ml of 50% solution) and/or intravenousthiamine (250 mg) as high potency intravenous Pabrinex where appropriateTreat acidosis if severe3 (0–60/90 minutes)Establish etiologyIdentify and treat medical complicationsPressor therapy where appropriate4 (30–90 minutes)Transfer to intensive careEstablish intensive care and EEG monitoringInitiate seizure and EEG monitoringInitiate intracranial pressure monitoring where appropriateInitiate long term, maintenance, antiepileptic therapyThese four stages should be followed chronologically; the first and secondwithin 10 minutes, and stage 4 (transfer to intensive care unit) in most settingswithin 60–90 minutes of presentation.*Derived from Shorvon 1994After assessment of these important conditions, and once therespiratory consequences of progressive neuromuscularweakness are established, the following requirements formanagement of critical neuromuscular diseases in ICU should befulfilled:1. Continuous monitoring of oxygen saturation to stay above95%; pacemaker to be considered if heart rate variability isabnormal.2. Assessment of muscle strength through measurement ofvital capacity, hand grip strength (dynamometer), armabduction time, head lifting time, loudness of voice, abilityto swallow secretions and use of accessory muscles ofventilation.
  49. 49. Brain Injuries | 493. Management of inability to swallow through frequentsuction, head positioning to allow use of a nasogastric, anorogastric or a Guedel tube.4. Assessment of cardiac output, e.g., in myositis andarrhythmias (autonomic fiber involvement in GBS),heparinization for prevention of deep venous thrombosis,care for decubital ulcers.5. Indications for intubation and artificial ventilation inneuromuscular critical cases: If oxygen saturation is below90% (below 85% if more chronic), exhaustive respiratorywork, forced vital capacity falling below 15 ml/kg andrecurrent minor aspiration, avoid use of muscle relaxants.If artificial ventilation is likely to be required for more thanapprox. seven days, a tracheostomy should be created andis more comfortable for the patient than continuedorotracheal intubation. Nutrition should be provided earlyvia a nasogastric tube. Strenuous efforts should be made toreduce the incidence of nosocomial infection. Patients withneuropathy should be monitored for autonomicdysfunction causing cardiac arrhythmia or fluctuatingblood pressure. Deep vein thrombosis should be avoided byregular passive limb movements and low-dosesubcutaneous heparin.6. Use assisted ventilation with IMV mode with low PEEP of 3cm H20 except in pneumonia, atelectasis and use as fewsedatives as possible to monitor neurologic findings(Murray 2002). Critical illness polyneuropathy andmyopathy are considered conditions associated withinflammatory injury to major organs involving peripheralnerves and skeletal muscles, and may add considerablevalue to the morbidity and mortality of the ICU stays.7. If systolic pressure remains below 90 mmHg after adequatevolume replacement, begin dopamine infusion to maintainsystolic pressure above 90 mmHg; if dopamine isinadequate maintain dopamine and start dobutamineinfusion. If the patient develops diabetes insipidus with
  50. 50. 50 | Critical Care in Neurologyurine output exceeding 250 ml/hour for 2 hours, start avasopressin infusion at a dose of 0.5-1.0 U/hour for adults,titrate infusion to maintain urine output at 100-200ml/hour. Send tracheal aspirate, urine and blood forroutine and fungal culture (Shoemaker 2000).Metabolic disturbances such as hypokalemia orhypermagnesemia should always be looked for and correctedfirst. In Guillain–Barré syndrome we recommend intravenousimmunoglobulin as being equally effective to plasma exchange,safer, and more convenient. In myasthenia gravis werecommend intravenous immunoglobulin followed bythymectomy or, where thymectomy is inappropriate or has beenunsuccessful, intravenous immunoglobulin combined withazathioprine and steroids. In polymyositis and dermatomyositis,steroids are the mainstay of treatment but intravenousimmunoglobulin is also effective.Management of subarachnoid hemorrhageSubarachnoid hemorrhage (SAH) is a complex medical andsurgical event. Among its multiple etiologies, one of the mostcommon relates to bleeding from a cerebral aneurysm. Theoptimal management of this life-threatening condition relies ona systematic and organized approach leading to the correctdiagnosis and timely referral to a capable neurosurgeon. Thefollowing is a brief summary of steps that should be initiatedwhen SAH is suspected, and the role of a medical neurocriticalcare facility.A CT scan should be obtained immediately after the diagnosis issuspected. If the CT scan is positive, lumbar puncture isunnecessary and even dangerous due to the risks of aneurismalrebleeding or transtentorial brain herniation. If the CT scan isnegative, lumbar puncture may be helpful if the history of theictal headache is not typical of subarachnoid hemorrhage,insidious in onset, or of migrainous character. If the patient
  51. 51. Brain Injuries | 51relates a history typical of SAH, a cerebral CT arteriogram shouldbe performed despite a negative CT scan. Up to 15% of CT scansobtained within 48 hours of SAH will be negative.Once the diagnosis is confirmed with a CT scan, a neurosurgeonwho can treat the patient should be contacted immediately.Delays in transfer may prove fatal because of the potential foraneurismal rebleeding prior to intervention. It is often best toallow the interventionist or surgeon who will be caring for thepatient to arrange for the diagnostic arteriogram to beperformed at the institution where the patient will undergointervention or surgery to repair the aneurysm. Arteriographyperformed by institutions infrequently treating SAH may betechnically inadequate and require repetition upon transfer tothe interventionist.Blood pressure must be closely monitored and controlledfollowing SAH. Hypertension will increase the chance ofcatastrophic rebleeding. Blood pressure control should beinitiated immediately upon diagnosis of SAH.Medical preoperative management includes prophylacticanticonvulsants, calcium channel blockade, corticosteroids, andantihypertensives as needed. We do not initiate antifibrinolytictherapy unless surgery is not considered within 48 hours of theinitial SAH.Medications that can be initiated prior to transfer tointerventionist or neurosurgeon include:– dexamethasone, 4 mg IV six hourly– nimodipine, 60 mg orally four hourly– phenytoin, 10 mg/kg IV load, then 100 mg orally/IV threetimes dailyA frequent source of diagnostic difficulty for theinterventionist lies in the use of excessive amounts of narcoticanalgesics prior to transfer to the neurosurgical service.Although pain control facilitates blood pressure control, theability to grade accurately the patient’s level of consciousnesshas significant impact on the timing of intervention. Clinical
  52. 52. 52 | Critical Care in Neurologygrading also, obscured by large doses of narcotic analgesics,makes surgical planning more difficult.
  53. 53. Basic Hemodynamic Monitoring of Neurocritical Patients | 535. Basic Hemodynamic Monitoring ofNeurocritical PatientsBassem Zarif, Magdy Khalaf, Nabil KitchenerThe importance of basic hemodynamic monitoring ofneurocritical patients comes from the goal of maintaining brainautoregulation. Brain autoregulation and other biological signalsare the variables to be monitored by using biomedical sensors.Complications that may occur in neurocritical patients (e.g.,sepsis, dehydration, post-cardiac arrest status) makehemodynamic monitoring of greater importance.The goals of hemodynamic monitoring in neurocritical careunits are to assess the magnitude of physiological derangementsin critically ill patients and to institute measures to correct theimbalance.The following steps should be taken to reach these goals.Although our review of data may be helpful, the attendingphysician should decide what to use and when to use it. Menu towork with for proper patient management:1. Pulse oximeter (SpO2) is regarded as one of the mostimportant advances in critical care monitoring. SpO2provides a continuous non-invasive method to measurearterial oxygen saturation, and should be used on everyneurocritical patient. The absorption spectra of both
  54. 54. 54 | Critical Care in Neurologyoxyhemoglobin and deoxyhemoglobin and thecharacteristics of pulsatile blood can thus be determined.SpO2 is accurate to within ± 2% for saturations >70%. SpO2 iswidely used in monitoring patients who have a variety ofneurological conditions (Adams 1997), and calculationsmade from the processed signals provide estimates of thetissue or venous and arterial blood and provide an estimateof the amount of oxygenated hemoglobin and the percentsaturation of hemoglobin by oxygen SaO2, which is not thesame as the PaO2 (partial pressure of oxygen) in the blood(Adams 1997). The PaO2 and SaO2 measurements ofoxygenation are related through the oxyhemoglobindissociation curve. Importantly, SpO2 is a measure ofarterial oxygenation saturation, not arterial oxygen tension(PaO2). Given the characteristics of the oxygen dissociationcurve, large fluctuations in PaO2 can occur despite minimalchanges in SpO2. In addition to its inability to measure PaO2,SpO2 provides no measure of ventilation or acid-base status.Therefore, it cannot be used to determine pH or arterialcarbon dioxide tension. Significant increases in arterialcarbon dioxide can occur with normal readings in SpO2.Although useful for arterial oxygen saturation, SpO2 shouldnot be assumed to provide information about ventilation.Studies have shown that to assure a saturation of 60 torr(8.0 kPa), an SpO2 of 92% should be maintained in patientswith light skin, whereas 94% saturation may be needed inpatients with dark skin. Oxygenation is consideredadequate if the arterial oxygen saturation is above 95%. Themajority of these patients are placed on positive endexpiratory pressure (PEEP) at 5cm H2O (Curley 1990).Also, for patients with manifestations consistent withhypoxemia (e.g., tachycardia, hypotension, anxiety, andagitation) there is a time delay in pulse oximeter to expressfluctuation in SpO2. Again in hypothermia, low CO2, andvasoconstriction secondary to drugs or peripheral hypoxia
  55. 55. Basic Hemodynamic Monitoring of Neurocritical Patients | 55all increase bias, imprecision, and response time forhypoxic episodes, so we proceed to the next step.2. Arterial blood gas analysis is widely available in hospitalsand offers direct measurements of many criticalparameters (pH, PaO2, PaCO2). Arterial blood gas analysis isamong the most precise measurements of oxygen tensionand pressure that will reflect tissue oxygenation (García2011).3. Non-invasive automated blood pressure devices arefrequently used to obtain non-invasive, intermittent bloodpressure measurements. Measurements of systolic anddiastolic pressure to calculate the mean arterial pressure(MAP) is mandatory to calculate the cerebral perfusionpressure. These devices are less accurate in critically illpatients as well as in those with secondary brain injury.These less accurate readings can distract the attention ofthe caregiver. The evaluation of blood pressure will besignificantly affected by the use of vasopressors. Therefore,the numeric reading may reflect vasoconstriction in spiteof decreasing perfusion with adequate blood pressure.4. Invasive blood pressure monitoring for continuousmonitoring and recording of the arterial pressure via anarterial catheter is preferable to the use of an automatedblood pressure device in hemodynamically unstablepatients (García 2011). The radial artery is most commonlycannulated because of its superficial location, relative easeof cannulation, and in most patients, adequate collateralflow from the ulnar artery. Other potential sites forpercutaneous arterial cannulation include the femoral,brachial, axillary, ulnar, dorsalis pedis, and posterior tibialarteries. Possible complications of intra-arterialmonitoring include hematoma, neurologic injury, arterialembolization, limb ischemia, infection, and inadvertentintra-arterial injection of drugs. Intra-arterial catheters arenot placed in extremities with potential vascularinsufficiency. However, with proper selection, the
  56. 56. 56 | Critical Care in Neurologycomplication rate associated with intra-arterialcannulation is low and the benefits can be important.5. A Foley catheter, for monitoring of urine output on anhourly basis or for 24 hours, is a simple and important toolto monitor volume status of the patient besides renalperfusion and function. The hourly urine output is a cheap,simple and indirect method of assessing adequacy ofcardiac output and tissue perfusion.6. A temperature probe is also indicated for purposes ofmonitoring core temperature.7. Continuous monitoring of volume status and otherparameters:If the patient is hypotensive, a fluid supplement with 1-2liters Ringer’s lactate for 30-60 minutes is reasonable.Subsequent fluid management should be based upon urineoutput and maintaining central venous pressure between 5and 10 mmHg. Monitor potassium, sodium, glucose andarterial blood gases every 4 hours. Especially if there isrespiratory embarrassment at initial evaluation,measurement of hematocrit, magnesium, blood ureanitrogen, creatinine, calcium, liver function tests, urineanalysis, prothrombin, partial thromboplastin times andphosphate levels are mandatory. If hematocrit is below30%, transfuse cross-matched blood (Amin 1993).8. Common indications for central venous cannulation:measurement of mean central venous pressure, large borevenous access, administration of irritating drugs and orparenteral nutrition, hemodialysis, placement of apulmonary artery catheter.Placement of a pulmonary artery catheter is indicated toobtain direct and calculated hemodynamic data that cannotbe obtained through less invasive means (Sakr 2005).The goal for all critically ill patients is to provideadequate oxygen for cellular use through suitable oxygenconsumption, which is variable between tissues, and thechanges of the basal or active metabolic rate for each cell.
  57. 57. Basic Hemodynamic Monitoring of Neurocritical Patients | 57Oxygen delivery to tissues and organs responds to manylocal systemic variables to keep cellular homeostasis.Pulmonary artery balloon flotation catheter insertion maybe necessary for full assessment of these parameters, and ofevaluation of determinants of cardiac output and theoxygen content of circulating blood, on which oxygendelivery is dependent. In the presence of positive pressureventilation with PEEP, central venous and pulmonaryartery occlusion pressures may be falsely elevated and needto be interpreted with caution. The fluid challenge is theonly way to interpret Central Venous Pressure (CVP) orPulmonary Artery Occlusion Pressure (PAOP).Assessment of the determinants of cardiac output willproceed as follows:a. Heart rate and rhythm assisted by pulse oximeter andelectrocardiogram.b. Preload assessed right and left heart; right heartthrough neck vein distension, liver enlargement andcentral venous pressure assessment; left heart throughdyspnea on exertion, orthopnea, arterial bloodpressure; pulmonary artery occlusion pressure andarterial pressure through waveform analysis (Sakr2005).c. Afterload assisted by mean arterial blood pressure andsystemic vascular resistance; contractility can beassessed by ejection fraction and echocardiography.As discussed earlier, the goal of hemodynamic monitoring inneurocritical care units is to assess the magnitude ofphysiological derangements in critically ill patients and toinstitute measures to correct the imbalance. Basic hemodynamicmonitoring consists of clinical examination, invasive arterialmonitoring, central venous pressure monitoring, hourly urineoutput, central venous oxygen saturation and echocardiography.Dynamic indices of fluid responsiveness such as the pulsepressure variation and stroke volume variation can guide
  58. 58. 58 | Critical Care in Neurologydecision making for fluid resuscitation. Cardiac output istraditionally measured using the pulmonary artery catheter; lessinvasive methods now available include the pulse contouranalysis and arterial pulse pressure derived methods. It isessential to determine whether the hemodynamic therapy isresulting in an adequate supply of oxygen to the tissuesproportionate to their demand. Mixed and central venousoxygen saturation and lactate levels are commonly used todetermine the balance between oxygen supply and demand(Walley 2011).
  59. 59. Neurocritical Monitoring | 596. Neurocritical MonitoringMervat Wahba, Nabil Kitchener, Simin MansoorNeurocritical care relies on monitoring cerebral functions.Intracranial pressure monitoring may indicate high pressure inseveral acute neurological conditions. Massive stroke may causelife-threatening brain edema and occur in about 10% of patientswith supratentorial stroke. Massive brain edema usually occursbetween the second and the fifth day after stroke onset. Casefatality rates may exceed 80%. Other neurologic conditions thatmay be accompanied with increased intracranial pressureinclude severe head injuries, status epilepticus, fulminanthepatic failure, Reye’s syndrome, and metabolicencephalopathies.Neuro-Specific MonitoringAccurate neurological assessment is fundamental for themanagement of patients with intracranial pathology. Thisconsists of repeated clinical examinations (particularly GCS andpupillary response) and the use of specific monitoringtechniques, including serial CT scans of the brain. This chapterprovides an overview of the more common monitoringmodalities found within the neurocritical care environment.
  60. 60. 60 | Critical Care in NeurologyIn general terms, a combination of assessments is more likelyto detect change than any one specific modality. Real-timecontinuous monitoring (e.g., measurement of intracranialpressure, ICP) will provide more timely warning about adverseevents (e.g., an expanding hematoma) compared to staticassessments such as sedation holds or serial CT brain scans.Clinical AssessmentThe Glasgow Coma ScaleThe Glasgow Coma Scale (GCS) provides a standardized andinternationally recognized method for evaluating a patient’s CNSfunction by recording their best response to verbal and physicalstimuli. A drop of two or more GCS points (or one or more motorpoints) should prompt urgent re-evaluation and a repeat CTscan.Eye opening is not synonymous with awareness, and can beseen in both coma and persistent vegetative state (PVS). Theimportant detail is that the patients either open their eyes to aspecific command or shows ability to fix eye on a specific targetor follows a visual stimulus.Pupillary responseChanges in pupil size and reaction may provide useful additionalinformation:– Sudden unilateral fixed pupil: Compression of the thirdnerve, e.g., ipsilateral uncal herniation or posteriorcommunicating artery aneurysm– Unilateral miosis: Horner syndrome (consider vascularinjury)– Bilateral miosis: Narcotics, pontine hemorrhage– Bilateral fixed, dilated pupils: Brainstem death, massiveoverdose (e.g., tricyclic antidepressants)In the non-specialist center, neurological assessment of theventilated patient consists of serial CT brain scans, pupillary
  61. 61. Neurocritical Monitoring | 61response, and assessment of GCS during sedation holds. Areduction in sedation level will usually be at the suggestion ofthe Regional Neurosurgical Center (RNC) and its timing willdepend upon a number of factors. Responses such as unilateralpupillary dilatation, extensor posturing, seizures, or severehypertension should prompt rapid re-sedation, repeat CT scan,and contact with the RNC. In the patient with multiple injuries,consideration must be given to their analgesic requirementsprior to any decrease in sedation levels.Invasive MonitoringCerebral perfusion pressure (CPP) reflects the pressure gradientthat drives cerebral blood flow (CBF), and hence cerebral oxygendelivery. Measurement of intracranial pressure (ICP) allowsestimation of CPP. CPP is mean arterial pressure minus ICP.Sufficient CPP is needed to allow CBF to meet the metabolicrequirements of the brain. An inadequate CPP may result in thefailure of autoregulation of flow to meet metabolic needs whilstan artificially induced high CPP may result in hyperemia andvasogenic edema, thereby worsening ICP. The CPP needs to beassessed for each individual and other monitoring modality (e.g.,jugular venous oximetry, brain tissue oxygenation) may berequired to assess its adequacy.Despite its almost universal acceptance, there are no properlycontrolled trials demonstrating improved outcome from eitherICP- or CPP-targeted therapy. However, in the early 1990sMarmarou et al. showed that patients with ICP valuesconsistently greater than 20 mmHg suffered worse outcomesthan matched controls, and poorer outcomes have beendescribed in patients, whose CPP dropped below 60 mmHg(Marmarou 1991; Juul 2000; Young 2003). As such, ICP- and CPP-targeted therapy have become an accepted standard of care inhead injury management.The 2007 Brain Trauma Foundation Guidelines (Brain TraumaFoundation 2007) recommend treating ICP values above
  62. 62. 62 | Critical Care in Neurology20 mmHg and to target CPP in the range of 50-70 mmHg. Patientswith intact pressure autoregulation will tolerate higher CPPvalues. Aggressive attempts to maintain CPP >70 mmHg shouldbe avoided because of the risk of ARDS.Table 6.1 – ICP ValuesNormal ICP <15 mmHgFocal ischemia occurs at ICP >20 mmHgGlobal ischemia occurs at ICP >50 mmHgUsual treatment threshold is 20 mmHgMeasuring ICPIntraventricular devices consist of a drain inserted into thelateral ventricle via a burr hole, and connected to a pressuretransducer, manometer, or fiber optic catheter. Althoughassociated with a higher incidence of infection and greaterpotential for brain injury during placement, this remains thegold standard. It has the added benefit of allowing CSF drainage.Historically, saline could be injected to assess brain compliance.Extraventricular systems are placed in parenchymal tissue, thesubarachnoid space, or in the epidural space via a burr hole.These can be inserted at the bedside in the ICU. These systemsare tipped with a transducer requiring calibration, and aresubject to drift (particularly after long-term placement).Examples of extraventricular systems are the Codman andCamino devices. These devices have a tendency to underestimateICP.In general, both types of device are left in situ for as short atime as possible to minimize the risk of introducing infection.Prophylactic antibiotics are not generally used.Indications for ICP monitoringIn any case of head injury, if brain CT is positive for pathology,and the patient fulfills the criteria for use of a ventilator,
  63. 63. Neurocritical Monitoring | 63monitoring for intracranial pressure (ICP) becomes mandatory.More specific indications are shown in Table 6.2.Table 6.2 – Indications for intracranial pressure (ICP) monitoring1) Traumatic brain injury, in particular:– Severe head injury (GCS <8)– Focal pathology on CT brain scan– Head injury and age >40– Normal CT brain scan but systolic blood pressure persistently <90 mmHg– Where other injuries and their treatment necessitate the use of sedationor anesthesia2) Subarachnoid hemorrhage with associated hydrocephalus3) Hydrocephalus4) Hypoxic brain injury, for example, after near-drowning5) Postoperative in patients at risk of severe cerebral edema6) Encephalopathy (e.g., in liver failure)Coagulopathy is the primary contraindication to insertion. TheICP device will generally be removed as soon as the patient isawake with satisfactory neurology (GCS motor score M5 or M6)or when physiological challenges (removal of sedation,normalizing PaCO2) no longer produce a sustained rise in ICP.Intracranial Pressure Waveforms and AnalysisThe normal ICP waveform is a modified arterial trace andconsists of three characteristic peaks. The “percussive” P1 waveresults from arterial pressure being transmitted from thechoroid plexi, the “tidal” P2 wave varies with brain compliance,whilst P3 represents the dicrotic notch and closure of the aorticvalve. It is important to establish the accuracy of the ICP traceand value before initiating therapy based upon the numbersgenerated. Transient sequential occlusion of the internal jugularveins or removing the head-up tilt should produce an increase inICP.
  64. 64. 64 | Critical Care in NeurologyThe ICP waveform: The ICP waveform can be divided intosystolic and diastolic components and demonstrates cardiac andrespiratory variations.– P1 (percussion wave): originates from pulsations in choroidplexus, sharp peak, consistent in amplitude– P2 (tidal wave): variable in shape, ends on dicrotic notch– P3 (dicrotic wave): begins immediately after dicrotic notchWhen ICP increases and compliance decreases, P2 and P3 elevatecausing a rounder waveform.In addition to simple pressure measurement, if ICP is recordedagainst time, a number of characteristic wave forms (Lundebergwaves) can be seen.– A waves: Pathological sustained plateau waves of 50-80mmHg lasting between 5 and 10 min, possibly representingcerebral vasodilatation and an increase in CBF response to alow CPP.– B waves: Small, transient waves of limited amplitude every1-2 min representing fluctuations in cerebral blood volume.These may be seen in normal subjects, but are indicative ofintracranial pathology when the amplitude increases above10 mmHg.– C waves: Small oscillations in ICP that reflect changes insystemic arterial pressure.With cerebral autoregulation intact, a rise in MAP producesvasoconstriction and a fall in ICP. However, when autoregulationfails, the circulation becomes pressure passive and changes in

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