(BQ) Part 1 book Textbook of neurointensive care has contents: Quality improvement and neurocritical care, quality improvement and neurocritical care, introduction to basic neuropathology, prehospital care of the neurologically injured patient,... and other contents.
A Joseph Layon Andrea Gabrielli William A Friedman Editors Textbook of Neurointensive Care Second Edition 123 Textbook of Neurointensive Care A Joseph Layon • Andrea Gabrielli William A Friedman Editors Textbook of Neurointensive Care Second Edition Editors A Joseph Layon, MD, FACP Critical Care Medicine Pulmonary and Critical Care Medicine The Geisinger Health System Danville PA USA Andrea Gabrielli, MD, FCCM Departments of Anesthesiology and Surgery University of Florida College of Medicine Gainesville FL USA Temple University School of Medicine Philadelphia PA USA William A Friedman, MD Department of Neurological Surgery University of Florida College of Medicine Gainesville FL USA ISBN 978-1-4471-5225-5 ISBN 978-1-4471-5226-2 DOI 10.1007/978-1-4471-5226-2 Springer London Heidelberg New York Dordrecht (eBook) Library of Congress Control Number: 2013945859 © Springer-Verlag London 2013 This work is subject to copyright All rights are reserved by the Publisher, whether the whole or part of the material is concerned, specifically the rights of translation, reprinting, reuse of illustrations, recitation, broadcasting, reproduction on microfilms or in any other physical way, and transmission or information storage and retrieval, electronic adaptation, computer software, or by similar or dissimilar methodology now known or hereafter developed Exempted from this legal reservation are brief excerpts in connection with reviews or scholarly analysis or material supplied specifically for the purpose of being entered and executed on a computer system, for exclusive use by the purchaser of the work Duplication of this publication or parts thereof is permitted only under the provisions of the Copyright Law of the Publisher's location, in its current version, and permission for use must always be obtained from Springer Permissions for use may be obtained through RightsLink at the Copyright Clearance Center Violations are liable to prosecution under the respective Copyright Law The use of general descriptive names, registered names, trademarks, service marks, etc in this publication does not imply, even in the absence of a specific statement, that such names are exempt from the relevant protective laws and regulations and therefore free for general use While the advice and information in this book are believed to be true and accurate at the date of publication, neither the authors nor the editors nor the publisher can accept any legal responsibility for any errors or omissions that may be made The publisher makes no warranty, express or implied, with respect to the material contained herein Printed on acid-free paper Springer is part of Springer Science+Business Media (www.springer.com) To my family—Susana Picado, Maria Layon-Taylor, Nicolas Layon, Daniel Layon—all in the service of our people and country All of whom have sacrificed To those who are in search of a home, family, country: may you find them To those who struggle to become: may you be —A Joseph Layon To my father Pietro and my mother Giuliana, now walking the family dog between the clouds, for being my role models and the inspiration behind all my efforts To my brother and friend Marco, the real smart guy of the family To my students, friends, and colleagues worldwide To our patients, our inspiration for compassionate care, our reason to try harder —Andrea Gabrielli To my many colleagues, friends, and patients who have taught me so much about neurosurgery —William A Friedman Foreword to the Second Edition During the years since the publication of the first edition of this Textbook of Neurointensive Care, considerable developments have evolved in the critical care of the neurologically injured patient This second edition captures such advances presented by more than 100 leading authorities, offering a clear and comprehensive update It represents a collective accomplishment of clinician scientists dedicated to providing such enormous material and thereby extensive knowledge in the care of the brain injured from the emergency department to the ICU, to the operating room, and through the postoperative period This edition is the only textbook providing such a comprehensive offering throughout the continuum of care Such a continuum of critical care is exemplified throughout this second edition in its extensive chapters A presentation of key concepts of brain physiology essential to the understanding of intracranial hypertension is offered in the chapter on elevated intracranial hypertension Despite recent advances in the treatment, diagnosis, and management of aneurysms and cerebral vasospasm, morbidity and mortality remain high and are addressed in the chapter on treatment of aneurysmal subarachnoid hemorrhage The chapter on intracranial hemorrhage is an essential presentation Such hemorrhage remains formidable as patient outcome is still poor, despite recent advances that have led to extensive research establishing evidence-based management This chapter notes the disparate incidence of stroke in African-Americans and discusses possible risk factors in this population Neuroradiologic imaging is discussed in a substantial chapter, providing an understanding of how such images are created utilizing MRI and CT modalities though technical presentation The chapter on pharmacotherapy in the neurosurgical ICU is a further example of the comprehensive approach to such care extended by this second edition Knowledge of pharmacokinetics and pharmacodynamics of neuroactive drugs is provided for the optimal management of neuroinjured patients In addition to these chapters, all the contributions provide evidenced-based data and algorithms for decision making and illustrate key points; multiple supporting references are provided for documentation and reviews This second edition is improved in its sectioning with the provision of an Introduction (Part I) which presents fundamentals of neurocritical care issues of organization, quality improvement, and the emerging ICU subspecialty of Neurointensive Care Medicine Part II addresses Neuroanatomy and Neurophysiology; Part III covers Neuromonitoring; Part IV addresses in detail the Neuroinjured Patient; Part V details Special Situations such as traumatic brain injury in the adult and as well as in the pediatric population, the treatment of spinal cord injury, and the treatment of seizures; Part VI provides Situations of Special Interest such as intraoperative neuroanesthesia, neurorehabilitation, and brain death and the management of potential organ donation This section also reviews the ongoing concerns of ethical issues in the neurointensive care unit In 2003, the year prior to the publication of the first edition of the Textbook of Neurocritical Care, the Joint Commission (JC, formerly JCAHO) launched the Primary Stroke Center Certification Program During the years since the First Edition, more than 925 certified primary stroke centers have been established in 48 states, with comprehensive stroke centers now being certified by JC in several states The Get With The Guidelines-Stroke National Quality Improvement and Registry Program of the American Heart/American Stroke Association has vii viii Foreword to the Second Edition grown rapidly over these years Over 1,400 hospitals are participating in this program The first edition of this textbook and its editors and authors have contributed immensely to the quality and outcomes of stroke care of these programs Interim and current developments so comprehensively provided now in this second edition will further enhance such care It is a pleasure and privilege to continue to work with such accomplished investigators This second edition is a tribute and an essential contribution to the care of the neurologically injured Danville, PA, USA Edgar J Kenton III, MD, FAAN, FAHA Preface to the Second Edition We claimed, in the Preface to the First Edition of Textbook of Neurointensive Care, that in the near future our hospitals would be composed of EDs, ICUs, and operating rooms Studies of hospitals seem to have borne this out And while we still are not sure of the precise dimensions and shape it will take, health care (maybe better put, health insurance) reform will impact our work and work environment significantly Even those of us who hoped for a reformed health system when the First Edition went to press had no idea, even in our heart of hearts, that in 2013 we would see the beginnings—just that—of the reform of our health-care system In this context, we have attempted to change and improve our Textbook of Neurointensive Care In this second edition, there is more emphasis on evidence-based medicine—our jumpoff point, not our end point—and best practice We have improved chapters on the organization of neurocritical care (Chap 1) and quality improvement (Chap 2); enhanced chapters on neuromonitoring (Chaps and 8) and on the prehospital care of the neurologically injured patient (Chap 9); and added chapters on neuroendocrine function (Chap 15), on hematological/ thrombotic issues (Chaps 16 and 17), and on acute kidney injury and the neurologically injured patient (Chap 19) Additionally, there is an entire chapter (Chap 36) on temperature regulation Finally, we have added a chapter on brain death and the management of the potential organ donor (Chap 44) The reader will note that we eliminated the section on “The Future of NeuroCritical Care.” We are good, but not that good! We cannot see into the future any better than anyone else can! We thank our contributors for their hard work We are in debt to them in a manner that will never be paid And the same goes for our editor and publisher, Elizabeth Corra and Grant Weston: they have the patience of saints Let us know what you think of this second edition As always, the errors in this book belong to the three editors Gainesville, FL, USA Gainesville, FL, USA Gainesville, FL, USA A Joseph Layon, MD, FACP Andrea Gabrielli, MD, FCCM William A Friedman, MD ix 526 ganglion cells which project via the optic nerve to the optic chiasm At this point, 53 % of these fibers decussate, and 47 % stay ipsilateral The optic tract terminates in the pretectal nucleus ipsilaterally, and this termination is located in the dorsal midbrain The pretectal nuclei project bilaterally to the Edinger-Westphal nuclei, which are the parasympathetic subnuclei of the oculomotor nerve The fibers decussate to synapse in the contralateral Edinger-Westphal nucleus and then travel through the posterior commissure [29] The Edinger-Westphal nucleus has cholinergic neurons that project to the ipsilateral ciliary ganglion, which in turn projects to the pupillary constrictor muscles in an ipsilateral fashion Understanding the neuroanatomy of this pathway can help to localize a neurological deficit If for example, the pupillary reaction is brisk and equal to direct and consensual response bilaterally, the entire system—including the optic pathways, the dorsal midbrain, the posterior commissure, the third nerve nuclear complex, the third nerve, and the pupillary constrictor muscles—are likely intact A frequently encountered examination finding in the NICU is that of asymmetric pupils The first step in approaching this patient is to determine which pupil is abnormal, the larger or smaller If a pupil is abnormally large because it fails to constrict, this usually is due to an intrinsic problem within the eye such as iris tears or synechiae or alternatively parasympathetic dysfunction If the smaller pupil is abnormal, this usually reflects sympathetic dysfunction such as a Horner’s syndrome This can be determined most easily by examining the patient in both brightly and dimly lit rooms In a brightly lit room, both pupils would be expected to constrict, so if the failure is that of pupillary constriction, the size difference between the two eyes would increase This would indicate that the larger pupil is the abnormal one In a dimly lit room, both eyes would be expected to dilate, so if the failure is that of dilation, the difference between the two eyes would be greater in this scenario This would indicate that the smaller pupil is abnormal [29] An alternative scenario is that of physiological anisocoria, which is usually less than 0.5 mm difference between pupils and the difference is equal in light and dark A frequently encountered examination finding is a dilated pupil that reacts poorly to direct or to a consensual response In some cases, however, whenever light is directed into a single-dilated pupil, the contralateral consensual response is normal This situation may be encountered when there is a compromised third nerve, which carries the efferent parasympathetic fibers from the Edinger-Westphal nucleus to the pupillary constrictor muscles The contralateral eye constricts to a consensual response, because the afferent limb made up of the optic nerve and tract remains intact [30] A “blown pupil” that is dilated and poorly reactive to light, especially when more severe than the oculomotor deficits encountered, indicates an extrinsic compression of the nerve B.D Riggeal et al This manifestation results because the parasympathetic fibers travel peripherally in the nerve and are usually more susceptible to compressive forces when compared to the oculomotor fibers that are located more centrally within the nerve The immediate concerns when faced with such an exam finding include an aneurysm, particularly of the posterior communicating artery, or alternatively a transtentorial herniation syndrome The motor function of the oculomotor nerve may be lost as the compression worsens and may involve the inner portions of the nerve, so as the patient has increasing dysfunction of the oculomotor functions; it can then be inferred that the intracranial process is worsening A compressive oculomotor nerve palsy can be caused by a few very important pathological processes including an aneurysm, particularly of the posterior communicating artery, as well as a transtentorial herniation syndrome [31] Because this is an emergent situation, it is important to obtain CNS imaging as quickly as possible A CT scan of the brain is usually adequate to rule out a transtentorial herniation, and a CT angiogram is required to evaluate properly for an aneurysm It has been shown that it is very important to have a properly trained neuroradiologist who understands the indication(s) for the study and laterality of the findings [32, 33] If the smaller pupil is abnormal, this usually indicates a failure of the sympathetic system in dilating the pupil Several conditions can account for this issue, but the one of particular concern is a Horner’s syndrome The Horner’s syndrome is characterized by the triad of miosis, anhidrosis, and ptosis This can be caused by a lesion anywhere along the central or peripheral pathways containing axons related to the oculosympathetic system If caused by a brainstem lesion, which is the main situation in which altered mental status can be associated with a Horner’s syndrome, there will often be a contralateral loss of pain and temperature sensation because the descending sympathetics travel in close proximity to the spinothalamic tract An ipsilateral ataxia and vertigo can be seen in cases of a lateral medullary syndrome A Horner’s syndrome can also be caused by lesions of the stellate ganglion as in the case of a pancoast tumor, or within the cavernous sinus, and/or as a result of a carotid dissection Pharmacological testing can confirm a Horner’s syndrome [34, 35] One to two drops of 0.5 % apraclonidine in each eye will result in a reversal of anisocoria in the case of a Horner’s syndrome This reversal is due to the weak alpha-1 agonist properties of this medication which cause a significant mydriasis in the Horner’s eye because of denervation hypersensitivity, and the strong alpha-2 properties that result in miosis in the unaffected eye [29, 36] If the pupils both react briskly to light and then both constrict weakly to contralateral stimulation, it is likely that the ipsilateral optic nerve is damaged [29] There may be a large differential diagnosis for an acute or subacute optic neuropathy, but the immediate primary concern when associated 23 Diagnosis and Treatment of Altered Mental Status with an altered mental status in the ICU would be preexisting damage to the optic nerve, demyelinating disease, or acute disseminated encephalomyelitis In the patient with HIV, the commonest optic neuropathy is caused by syphilis The corneal reflex is a monosynaptic connection comprised of two cranial nerves and connections within the pons The afferent limb is the nasociliary branch of cranial nerve V1 When the cornea is touched with a sterile cotton swab, this signal travels into the brainstem at the level of the pons, descends to the caudal pons, and terminates in the bilateral facial nerve motor nuclei The motor nucleus of VII projects ipsilaterally to the muscles of facial expression resulting in contraction of the orbicularis oculi bilaterally when either cornea is touched If only one side of the face blinks when either cornea is touched, this indicates a peripheral facial nerve lesion on the side of decreased orbicularis oculi contraction If both sides of the face manifest a decreased blink when one cornea is touched, but both contract normally when the other is touched, it is likely that there is either damage to the peripheral trigeminal nerve or to the fascicle that contains the fibers descending to the bilateral motor nuclei of VII If the fascicle is damaged, it is common to have an exaggerated jaw jerk reflex (often evidence of a pontine issue and corticobulbar dysfunction) [37] A patient may hold their jaw loosely open while an examiner places their finger on the chin and lightly strikes their own finger with a reflex hammer The patient’s jaw should normally gently recoil, but with an exaggerated jaw jerk, this becomes hyperactive and the patient may in some cases click their teeth together The brainstem connections in the lower pons and upper medulla can be tested by using the vestibulo-ocular reflex The vestibulo-ocular reflex can be tested by performing a rapid head movement test, effectively turning the patient’s head from side to side and observing for contralateral eye movement as well as nystagmus This examination maneuver has been famously called a “doll’s eyes” maneuver because the eye movements resemble that of an old fashioned doll that would move with head turning In this circuit [38, 39], the vestibular systems project to the vestibular nuclei, which in turn stimulate the abducens nucleus on the side opposite the direction of head rotation and in turn inhibit the abducens nucleus on the side in which the head is turning The abducens nucleus then projects via the abducens nerve to the ipsilateral lateral rectus and also, via the median longitudinal fasciculus, to the contralateral medial rectus subnucleus of the oculomotor complex These eventually stimulate the medial rectus on the homolateral side The connections result in both eyes moving in the direction opposite of head rotation A diagram of these important eye movements is shown in Fig 23.1 If the patient is awake, the vestibulo-ocular reflex is usually suppressed due to cortical projections overriding the internuclear mechanisms If the patient is comatose and these systems remain intact, the eyes 527 L R Slow Slow III III VI VI PPRF PPRF VIII VIII Fig 23.1 Diagram of important eye movements in an examination maneuver that has been famously called a “doll’s eyes” maneuver should move conjugately in the direction opposite the head rotation [40] Prior to performing this test, particularly in cases of trauma, it should be confirmed that the cervical spine is stable An alternative method, by which these systems can be tested, especially when the cervical spine is unstable, is to employ caloric testing [30, 41] This can be performed with either warm or cold water, but cold water is usually utilized as it provides a more potent stimulus After ensuring that the tympanic membrane is intact, the ear canal is irrigated with cold water The typical response is for both eyes to slowly move in the direction toward irrigation In a conscious patient, or in one with intact cerebral hemispheres, a fast corrective eye movement back toward primary position should manifest The repetitive slow eye movements toward the irrigated ear and the fast movements away result in a phenomenon referred to as nystagmus Since nystagmus is named for the fast phase, cold-water calorics result in nystagmus beating in the opposite direction of the irrigated ear This can be easily remembered by the mnemonic “COWS.” This stands for cold-opposite, warm-same An internuclear ophthalmoplegia, which is a disruption of the medial longitudinal fasciculus, can also be identified by a careful eye exam when the adducting eye does not move fully medially, and the abducting eye either does not move past midline or has slowed saccades such that the eyes are dysconjugate [39] This maneuver can also aid in localizing the lesion to the dorsal pons/midbrain In a comatose patient, the vestibulo-ocular reflex can be utilized to evaluate for this phenomenon Obtaining the gag reflex is accomplished by pressing a sterile tongue blade or cotton swab against the oropharynx region and by observing for symmetric palatal elevation 528 without uvula deviation The afferent limb of this reflex is largely mediated by cranial nerve nine, which terminates in the nucleus solitaries and the efferent limb, which is largely cranial nerve X originating in the nucleus ambiguus This reflex indicates cranial nerve ten dysfunction, especially if the palate elevates asymmetrically and/or if the uvula deviates away from the side of weaker palate elevation A weak gag reflex without asymmetric palate elevation or uvula deviation can indicate a cranial nerve nine lesion, but it can also be seen in perfectly normal individuals since up to one third of healthy people have an absent gag reflex [42] Funduscopic Examination The funduscopic examination is an often overlooked portion of the physical examination in a patient with altered mental status, yet it can provide some important clues to the diagnosis or clues to associated conditions The funduscopic examination is accomplished with either an indirect or more commonly a direct ophthalmoscope Commonly in the ICU setting, the pupils can be quite small, making the fundus difficult to visualize A better examination can be achieved by applying mydriatic eye drops, either using a sympathomimetic like phenylephrine or an anticholinergic such as tropicamide It is extremely important, especially in patients with alteration of consciousness, to document in the chart what kind of dilation you have performed, what time the dilation was performed, and to ensure that you dilate both eyes equally Failure to so could result in the inappropriate assumption that the patient could have a compressive third nerve palsy, and this could lead to unnecessary imaging studies and/or possibly even interventions, both of which could pose potential harm to the patient To perform the direct funduscopic examination, the direct ophthalmoscope is held next to the examiners eye, and light is directed into the patient’s eye A red reflex is found, and this represents the reflection of light bouncing off of the choroidal membrane This red reflex is followed, while the examiner advances the ophthalmoscope closer to the patient’s pupil until vessels are observed Once the vessels are found, they are followed back to the optic disk to observe for any abnormalities, particularly optic disk edema Once the optic disk is visualized, the remainder of the retina and vasculature is visualized If the margins of the optic disk are indistinct, optic disk edema could be present but must be distinguished from the pseudoedema caused by a tilted disk, optic disk drusen, and other potential causes If optic disk edema is present, it could be the result of increased intracranial pressure, in which case the edema observed is called papilledema True optic disk edema that is not caused by increased intracranial pressure includes: optic neuritis associated with demyelinating disease, certain infectious etiologies, or some vascular causes Papilledema, caused by increased intracranial pressure, can be a result of multiple etiologies including B.D Riggeal et al brain neoplasm, infections such as meningitis or abscess, cerebral sinus thrombosis, idiopathic intracranial hypertension, or any other intracranial space occupying lesion Optic disk edema uncommonly results from an acute process other than increased intracranial pressure such as a subarachnoid hemorrhage The retinal vessels should also be inspected for attenuation, embolus, or evidence of cuffing, which can indicate CNS vasculitis Hollenhorst plaques are bright, yellow, refractile plaques made of cholesterol in the retinal arterioles [43] These indicate embolic disease, possibly from the internal carotid artery, which would corroborate carotid disease in cases of anterior circulation ischemic events Motor The motor examination should include descriptions of bulk, tone, and strength, as well as observations of any abnormal hypo- or hyperkinetic movements In a patient manifesting an altered mental status, this examination may prove to be a challenge Patients may not follow commands, or alternatively they may be intubated, sedated, or paralyzed When it is not possible to grade strength formally, tone and asymmetry of spontaneous movements can be observed, as well as potentially abnormal postures (such as external rotation of a weak lower extremity) Typically, with a peripheral nervous system lesion, tone is decreased, and with a central nervous system lesion, tone is increased An exception to this is in cases of spinal pathology, when in the acute setting, the patient may have a flaccid paralysis, the so-called “spinal shock” syndrome [44] Another portion of the motor examination is observation of the response to a painful stimulus One example is when the trapezius is squeezed with enough force to result in pain, and the pain elicits a movement A response to pain that would indicate at least partial preservation of neurological function would be for the patient to reach toward the source of the noxious stimulus, which would be a localizing and an appropriate response [30] If there is a significant disruption of the motor systems above the level of the midbrain, the inhibition of the rubrospinal tract by the corticospinal systems is released, and the patient will usually exhibit decorticate posturing, which is elbow flexion, forearm supination, and wrist and finger flexion If there is significant damage to the motor systems below the red nucleus, the rubrospinal tract is also affected, and therefore the tract that provides the dominant tone is the vestibulospinal tract, and this response results in decerebrate posturing, which is extension at the elbow, pronation of the forearm, and extension of the wrist [3] Basal Ganglia Examination Hyperkinetic movements (e.g., tremor, chorea) or hypokinetic movements (e.g., parkinsonism) should clue the clinician to the possibility of basal ganglia dysfunction An MRI study and possibly follow-up laboratory analysis may be 23 Diagnosis and Treatment of Altered Mental Status necessary Clinicians should be aware of the chorea syndrome that may appear during diabetic ketoacidosis and also the chorea and other movement disorders that may appear as a result of liver, thyroid, or metabolic dysfunction Finally, abrupt withdrawal of dopamine (Sinemet) can result in the neuroleptic malignant syndrome and should be avoided The use of neuroleptic medications can exacerbate or unmask basal ganglia features and should be avoided if possible in ICU patients 529 a painful stimulus to each extremity, and if the patient responds to this pain, it is inferred that, grossly, the anterolateral system known as the spinothalamic tract may be intact Testing for neuropathy, radiculopathy, plexopathy, or other issues may require a more intact mental status Laboratory Workup Complete Blood Count (CBC) Reflex Examination Abnormal reflexes are an important adjunct to the motor examination, particularly when accompanied by weakness The reflexes may help to determine if the weakness is central or peripheral in origin If a central nervous system lesion is present, the inhibition on the alpha motor neuron in the anterior horn cells of the spinal cord will be released, and there would be hyperexcitablity of the myotatic stretch reflex When the tendon is tapped with a reflex hammer, the primary afferent fibers directly synapse on the motor neuron that supplies the attached muscles Given that the descending inhibition on these neurons is released, the resulting contraction of the muscles is exaggerated If a peripheral lesion is present, the reflex may be decreased, although the afferent limb of the stretch reflex is intact If the motor neuron is damaged, the muscle cannot contract with full force, resulting in hyporeflexia [45] The Babinski response is also a useful part of the motor examination In testing the Babinski response, the lateral aspect of the plantar surface of the foot is scratched hard enough to produce a noxious stimulus If the first movement of the great toe is upward, this is a Babinski sign Experimental data in mice and humans indicate that this response results from damage to the medullary reticulospinal tract; however, in clinical practice, it is used to identify individuals simply with potential CNS damage [30, 46, 47] Cerebellar Examination The cerebellar examination is often difficult to test in an ICU setting and especially with an altered mental status When present, cerebellar findings may be clues to posterior fossa lesions that may progress to include compromise of the ARAS in the brainstem and eventually cause depressed consciousness Cerebellar findings include appendicular ataxia, dysmetria, rebound, dysdiadochokinesia, rhythm problems, and, in select cases, associated tremor In the more mobile patient truncal titubation, wide-based gait, and eye movement abnormalities may be present with more midline and anterior cerebellar lesions [13, 30, 45] Sensation The sensory examination can be tricky in the ICU and even trickier in the setting of AMS It is extremely subjective A crude way of testing sensation in this setting is to provide The CBC can be helpful in cases of altered mental status for several reasons A leukocytosis can indicate an infectious or neoplastic process, either of which can cause confusion, particularly in patients with decreased functional cognitive reserve This does not exclude a CNS structural process as the cause, but it can be useful in pointing a clinician in a different direction A low hemoglobin and hematocrit, indicating anemia, either may be completely unrelated to the altered mental status or can be symptoms of a systemic process causing the altered mental status such as a microangiopathic hemolytic anemia or can worsen cognition in patient with decreased cognition at baseline such as encountered in dementing illnesses [48, 49] Thrombocytosis can either indicate a neoplastic process or could be reactive and support an infectious/inflammatory diagnosis Thrombocytopenia can be seen in multiple conditions but particularly in microangiopathic hemolytic anemias [50] and disseminated intravascular coagulopathy, both of which can cause altered mental status Chemistries Patients manifesting an acute confusional state/delirium or coma should at a minimum have a complete metabolic panel performed Often, hyponatremia, diabetic ketoacidosis, acute uremia, and hepatic encephalopathy can be quickly uncovered Also, certain treatable issues such as hypercapnia due to pulmonary insufficiency may result in an impairment of consciousness that requires ICU monitoring Early treatment aids in prevention of complications and potentially death Further workup is usually warranted to find the underlying etiology causing any metabolic disturbance Elevated ammonia levels can be encountered in the setting of severe liver damage and also as a result of medications such as valproate, which can also be associated with encephalopathy [51] Often, if you treat the underlying etiology of the hyperammonemia, the encephalopathy can resolve An example of this is decreasing the dosage of valproate or discontinuing it may be indicated if this is found to be the underlying cause Treatment with lactulose, which is the mainstay of treatment, can increase the gastrointestinal 530 excretion of ammonia and may speed the reversal of alterations in mental status, but the evidence here is lacking [52] Neuroimaging The history and examination should guide the clinician to a localization and, subsequently, an appropriately limited differential diagnosis Based on this, imaging of the central nervous system may be warranted Several modalities are available, each having advantages and disadvantages The most pertinent imaging studies in most cases include CT and MRI of the brain The advantage of CT is that it is fast, readily available, and less susceptible to movement artifact, while with MRI, the images are usually better quality, more sensitive in detecting pathology, and will usually give more information about a specific etiology Selecting which study to utilize should vary depending on the clinical scenario encountered CT Computed tomography (CT) of the brain is a fast and extremely efficient way to evaluate for structural abnormalities in a patient with an AMS Especially in cases of an acute stroke, intracerebral hemorrhage, subdural hematoma, or epidural hematoma, the brain CT is very useful to quickly ascertain an underlying cause for an AMS CT has an excellent spatial resolution [53, 54] but lacks the contrast resolution of MRI, which often makes it an inferior modality if searching for lesions within the CNS B.D Riggeal et al the ICU setting or potentially warrant a surgical or endovascular intervention Acute thalamic infarcts interrupting the reticular activating system may result in an alteration in mental status, which may not be seen on CT imaging; these also sometimes respond to dopamine or dopamine agonist therapy and manifest with fluctuating levels of consciousness The clinician should never hesitate to use a brain CT, MRI, or potentially both tests to uncover the etiology of any case of AMS, especially when the history and examination not point clearly to the etiology Neurodiagnostics Lumbar Puncture The lumbar puncture is particularly important in the altered mental status workup, especially if an infectious etiology is suspected, if the patient is immunocompromised, or if a diagnosis remains elusive after an initial workup Sampling of the CSF allows for evaluation of the chemical composition, quantification of the number of erythrocytes and leukocytes, culture of the fluid, polymerase chain reaction for DNA of infectious organisms, evaluation of abnormal cells, and detection of the presence of abnormal proteins such as specific antibodies The spinal needle can also be attached to a manometer so that the CSF pressure can be measured A normal CSF constitution is less than five leukocytes without any polymorphonuclear cells, no erythrocytes, 15–50 mg/ dL of protein, and a glucose concentration that is about 2/3 that of the serum glucose; it is important to get a peripheral blood stick at the exact time of the LP [55] A description of the commonly found values in some infectious CSF processes is depicted in Table 23.3 MRI Magnetic resonance imaging (MRI) of the brain can be particularly useful for the evaluation and further characterization of lesions that may cause AMS (stroke, hemorrhage, venous issues, intracranial hypotension) The evaluation of posterior fossa lesions causing alterations in mental status is particularly useful as some of these etiologies may not be adequately imaged on CT MRI is particularly important to fully characterize lesions, their appearance, involvement of adjacent structures (or lack thereof), and patterns of appearance on the various sequences, all of which aid in making a diagnosis The excellent contrast resolution is quite useful in MRI given that many lesions within the CNS are often of similar density, resulting in similar contrast, and thus may be missed by CT scan In acute stroke, the diffusion-weighted MRI is quite useful In this condition, the brain CT may be normal early, and the diffusion-weighted MRI will show an acute brainstem infarct that may require close observation in EEG The electroencephalogram (EEG) is commonly performed in the critical care setting, especially in patients with nonconvulsive status, where clinical presentation may prove hard to decipher Continuous EEG monitoring in the ICU allows the physician to monitor the progress of antiepileptic treatment and to decide whether or not the patient will require more aggressive management EEG is commonly abnormal in the setting of an alteration of consciousness and can offer clues as to elusive diagnoses [56] EEG is particularly useful in situations in the ICU when the patient is delirious or having an AMS, and the history is unable to be obtained It is common that patients with delirium from a metabolic disturbance, hypoglycemia, diabetic coma, or excess use of sedatives will have a slowing of the posterior dominant rhythm which is normally in the alpha frequency In patients with hepatic 23 531 Diagnosis and Treatment of Altered Mental Status Table 23.3 Commonly found values in some infectious CSF processes in lumbar punctures Component WBC Cell-type predominance Glucose Protein Viral 40 Often normal or mildly elevated Bacterial >1,000 Mostly neutrophils