(BQ) Part 2 book The practice of emergency and critical care neurology has contents: Management of specific disorders in critical care neurology, management of systemic complications, postoperative neurosurgical and neurointerventional complications, formulas and scales,... and other contents.
PART VII Management of Specific Disorders in Critical Care Neurology http://internalmedicinebook.com http://internalmedicinebook.com 26 Aneurysmal Subarachnoid Hemorrhage M ajor medical institutions may admit 50–75 patients with an aneurysmal subarachnoid hemorrhage (SAH) a year A multidisciplinary team is required to respond to the immediate needs of the patient and to plan for repair of the aneurysm.8,42,101,154,175 Expertise may prevent poor outcome.25,47,133 After aneurysmal rupture, 10% of patients die suddenly or within the first hours before ever receiving adequate medical attention Many of these patients had marked intraventricular extension of the hemorrhage and acute pulmonary edema, both reasons for sudden death.144 Of those most severely affected who reach the emergency department (ED) or neurosciences intensive care unit (NICU), half die within months Some of these patients may have been found pulseless and required prolonged cardiopulmonary resuscitation Patients who survive a major first rupture face the immediate risk of catastrophic rebleeding, rapidly developing hydrocephalus, potentially life- threatening pulmonary edema, and cardiac arrhythmias Presentation in a poor clinical condition often indicates that the hemorrhage is not confined to the subarachnoid space but rather there is intraventricular and intraparenchymal extension Many have additional large ventricles and are in need of CSF diversion with a ventriculostomy The critical steps in managing SAH are to surgically clip the aneurysm or occlude the sac by inserting platinum coils, to treat clinical neurologic deterioration early, and to manage major systemic complications.169 Aneurysmal subarachnoid hemorrhage is a prime example of a neurocritical and neurosurgical disorder where outcome in the first days after presentation cannot be judged adequately and care of the initially comatose patient can lead to a satisfactory outcome Fortunately, a considerable proportion of patients with SAH present with severe headache and are alert with little other findings Early repair of the aneurysm may result in an excellent outcome CLINICAL RECOGNITION The incidence of aneurysmal SAH varies, but overall is 10 cases per 100,000 persons per year (doubled in Finland and Japan).112 The risk is nearly two times higher in women (particularly with smoking history) than in men and in blacks than in whites Subarachnoid hemorrhage is more common in patients with a family history of SAH,101 polycystic kidney disease, systemic lupus erythematosus, or Ehlers-Danlos disease (Capsule 26.1).60,61 Aneurysmal SAH may be manifested in many ways Typically, an unexpected instantaneous headache warns the patient of a very serious disorder and is often described as excruciating and overwhelming113 (Chapter 4) Vomiting may occur several minutes into the ictus as a result of further distribution of blood throughout the subarachnoid space Profuse vomiting may override the headache and has been mistaken for a “gastric flu” by the patient or initially consulted physician With an incomplete medical history and no inquiry about acute headache, patients may be wrongly transferred to a medical ICU (cardiac resuscitation and pulmonary edema), gastrointestinal service (vomiting), or coronary care unit (cardiac arrhythmias with new electrocardiographic [EKG] changes) Other unusual clinical presentations have included acute paraplegia (anterior cerebral artery aneurysm rupture into frontal lobes) and severe thoracic and lumbar pain caused by meningeal irritation These presentations may have resulted in a delay in cranial computed tomography (CT) scan imaging The abruptness of the headache is not specific for SAH; it may occur in conditions such as arterial dissection, pituitary apoplexy, hypertensive encephalopathy, spontaneous intracranial hypotension, and cerebral venous thrombosis43,44,143 (Chapter 4) Some patients briefly lose consciousness Inappropriate behavior and agitation or drowsiness may follow Localizing neurologic findings, although transient, may indicate the http://internalmedicinebook.com 318 Part VII: Management of Specific Disorders CAPSULE 26.1 ANEURYSMAL RUPTURE What causes aneurysms to rupture is puzzling Risk factors have included recently documented enlargement (rupture of aneurysms < mm is uncommon; most ruptured aneurysms are 7–8 mm, and risk of rupture increases significantly in aneurysms of ≥ 10 mm),88 hypertension, cigarette smoking, and family history of aneurysms and SAH Aneurysmal rupture has been reported to have occurred during weightlifting, sexual orgasm, and brawling, events that suggest acute hypertensive stress on a thin aneurysmal wall.160 However, at least 50% of patients have SAH while at rest Seasonal changes have been implicated with increased rupture rate during colder temperatures and influenza peaks An association between a recent infection and aneurysmal rupture has not been definitively established, but is plausible Intracranial pressure rises dramatically to at least the level of the diastolic blood pressure, causing cerebral perfusion standstill The increase in intracranial pressure decreases within 15 minutes but may persist if acute hydrocephalus or a shift from intracerebral hematoma has occurred Rupture stops within 3–6 minutes after ejection of up to 15–20 mL/min into the basal cistern Hemodynamic variables have been tested on cadaver and computer models Variables that may determine rupture are wall shear stress, intra-aneurysmal flow velocity, and inflow jet and angles of entry and vortexes Wall sheet stress is caused by the frictional force of blood, and areas with high forces may fragment the internal elastic lamina and cause blebs and aneurysms.56,148 Hemodynamic stress may cause morphologic changes involving the endothelial lining of the walls, with intimal hyperplasia, and organizing thrombosis Many ruptured vacular aneurysms show inflammatory changes, with infiltrating leukocytes and macrophages promoting fibrosis Other theories focus on the multitudes of vortices or unstable flow High inflow jets with large impact zones may result in thrombus or daughter sac formation.20,21 VORTEX FORMATION DAUGHTER SAC Subarachnoid hemorrhage Left: aneurysmal rupture causing diffuse subarachnoid hemorrhage Right: Vortex formation in aneurysm site of the ruptured aneurysm For example, patients with a ruptured middle cerebral artery (MCA) aneurysm may have transient or persistent aphasia In patients with a ruptured MCA aneurysm and intraparenchymal extension, hemiparesis often is found Abulia most often occurs as a complication of a rupture of an aneurysm of the anterior cerebral artery (ACA) Generalized http://internalmedicinebook.com Chapter 26: Aneurysmal Subarachnoid Hemorrhage 319 and vitreous hemorrhages Top: Subhyaloid hemorrhage in subarachnoid hemorrhage Bottom left: Red reflex is absent from vitreous hemorrhage also known as Terson syndrome Bottom middle: Improvement in vision Bottom right: Normal red reflex as shown by retro illumination with fundus camera FIGURE 26.1: Subhyaloid tonic-clonic seizures are not quite so often seen at the time of rupture, and it is possible that extensor posturing or brief myoclonic jerks with syncope at onset may be mistaken for a seizure These clinical features in SAH are identical whether or not an aneurysm is detected Different presentation is expected, however, in an established benign variant of nonaneurysmal SAH, so-called pretruncal or perimesencephalic SAH The patients are almost exclusively alert Loss of consciousness is seldom observed and seizures are absent, and the onset of headache is less acute—in minutes rather than a second Neurologic examination reveals neck stiffness in most patients, except those seen early after the initial event and those who are comatose Nuchal rigidity can be demonstrated by failure to flex the neck in the neutral position and failure of the neck to retroflex when both shoulders are lifted Retinal subhyaloid hemorrhages are present in approximately 25% of the patients (Figure 26.1) (This syndrome is more often observed in comatose patients and after rebleeding.) These flat-topped hemorrhages occur when outflow in the optic nerve venous system is suddenly obstructed by the intracranial pressure (ICP) wave.55 Visual loss may be severe, with perception of light or hand motion only, if the hemorrhage expands and ruptures into the vitreous (Terson syndrome).131 Cranial nerve abnormalities occur infrequently in SAH unless a giant basilar artery aneurysm (third-or sixth-nerve palsy) or a large carotid artery aneurysm (chiasmal syndromes) directly compresses surrounding structures The pupil is dilated and unreactive to light in a third-nerve palsy because of compression of the exteriorly located fibers that form the light reflex However, up to 15% of posterior communicating artery aneurysms may occur with a pupil-sparing third-nerve palsy Aneurysm of the basilar artery may produce unilateral or bilateral third-or sixth-nerve palsy.87 If the basilar artery aneurysm enlarges and progressively compresses the oculomotor nuclei of the pons, horizontal gaze paralysis, skew deviation, internuclear ophthalmoplegia, and nystagmus occur, commonly in association with long-tract signs such as hemiparesis and ataxia Occlusion of the proximal posterior cerebral artery, often encased in a giant aneurysm, may occur, causing either classic Weber syndrome (Chapter 30) due to mesencephalon infarction (third-nerve palsy with opposite hemiparesis) or homonymous hemianopia due to occipital lobe infarction In comatose patients, a certain eye position may be localizing These forced gaze positions include downward gaze and wall-eyed bilateral internuclear ophthalmoplegia, and are characteristically seen with acute hydrocephalus (Figure 26.2).90 Hemiparesis that usually involves the face, arm, and leg should point to an intracranial hematoma in SAH An anteriorly placed intracranial http://internalmedicinebook.com 320 Part VII: Management of Specific Disorders FIGURE 26.2: Wall- eyed bilateral internuclear ophthalmoplegia with acute hydrocephalus in patient with aneurysmal subarachnoid hemorrhage hematoma in the frontal lobe may not produce motor weakness but may be associated with agitation and bizarre behavior Many patients are confused, and may ramble nonsensically Korsakoff syndrome with impaired recall and fabrications may occur in ruptured anterior communicating aneurysm Abulia, a general sense of disinterest, and lackluster attention are also features, becoming apparent days later.62 Temporal lobe hematoma in the dominant hemisphere may produce aphasia, but often associated mass effect and brainstem displacement decrease the level of consciousness and word output Generalized tonic-clonic seizures are accompanied by aneurysmal rupture in 10% of patients, or these appear during rebleeding These “seizures” are likely ischemic in nature and a result of a major increase in ICP Nonconvulsive status epilepticus may occur, and the clinical signs are difficult to differentiate from the effects of initial rupture However, in our experience, electroencephalography (EEG) has rarely documented nonconvulsive status epilepticus Epilepsia partialis continua is equally uncommon in aneurysmal SAH It is more common in patients with additional subdural hematoma and when delayed cerebral infarction occurs Systemic manifestations may include respiratory failure and oxygen desaturation from aspiration, pulmonary edema, or obstruction of the airway Cardiac arrhythmias may involve the entire spectrum of supraventricular and ventricular arrhythmias Most of the time they are associated with EKG changes, which may simulate or indicate acute myocardial infarction Elevated troponin I levels may occur in approximately 25% of the cases seen on the first day Major cardiac arrhythmias may lead to cardiac resuscitation after SAH and generally portend poor outcome, but patients may improve substantially.152 When patients are comatose at presentation, it is largely due to the initial rise in ICP with reduction of cerebral blood flow and, as a consequence, diffuse bihemispheric ischemia.79 However, one should try to make a distinction between the direct effects of the initial impact and early neurologic deterioration due to other causes Acute hydrocephalus may have developed in the interim, and placement of a ventricular drain could markedly improve the level of consciousness Patients admitted days after the ictus may have symptomatic cerebral vasospasm, and focal signs and symptoms may not be present Coma may be caused by brain tissue shift from a large expanding hematoma in the sylvian fissure Removal of the hematoma and repair of the aneurysm may result in marked improvement The clinical course in poor-grade aneurysmal SAH is unpredictable in the first 24–48 hours Patients moribund at presentation may improve in a matter of hours without much neurosurgical or medical intervention, although the prognosis may remain guarded Systemic metabolic factors may contribute, and each of them should be excluded Measurements of arterial blood gas, electrolytes, and serum glucose must be obtained rapidly in every patient with SAH who enters the NICU A simple clinical grading system proposed by the World Federation of Neurological Surgeons (WFNS) introduced the Glasgow Coma Scale in SAH grading46,139 (Table 26.1), and for practical reasons the severity is graded as good (WFNS I–III) or poor (WFNS IV or V) A correlation between outcome and initial grading level exists This rather crude scale may also guide the timing TABLE 26.1 GRADING SYSTEM PROPOSED BY THE WORLD FEDERATION OF NEUROLOGICAL SURGEONS FOR THE CLASSIFICATION OF SUBARACHNOID HEMORRHAGE WFNS Grade Glasgow Coma Scale Score Motor Deficit I II III IV V 15 14–13 14–13 12–7 6–3 Absent Absent Present Present or absent Present or absent WFNS, World Federation of Neurological Surgeons http://internalmedicinebook.com Chapter 26: Aneurysmal Subarachnoid Hemorrhage (a) (b) (c) (d) 321 FIGURE 26.3: Subarachnoid hemorrhage (a, b) Subarachnoid hemorrhage with complete filling of the basal cisterns and fissures (arrows), creating a “crab-like” cast (c) Global cerebral edema (d) Extensive low-attenuation changes (arrows) in frontal and insular cortex of surgery Some neurosurgeons defer craniotomy for aneurysmal clipping in patients with WFNS V, but coiling may proceed Improvement in grade may make the patient eligible for aneurysmal clipping N E U R O I M AG I N G A N D L A B O R AT O R Y T E S T S Subarachnoid hemorrhage shows on CT scan (Figure 26.3a and b) Some patients show CT scans with massive SAH and early global edema (Figure 26.3c and d).27 CT perfusion may show reduced blood flow These findings are more common in patients who remain comatose after cardiopulmonary resuscitation When CT scan is done within hours after the event, the sensitivity in aneurysmal SAH is very high and may approach 95% In 2%–5% of the patients, subarachnoid blood has completely “washed out” on CT scans within 24 hours, but more likely, CT may have missed a thin layer of blood Repeat CT scan in patients with initial “negative CT” and xanthochromia often documents traces of SAH in sulci or ventricles.54 http://internalmedicinebook.com 322 Part VII: Management of Specific Disorders Fisher developed one of the first grading systems for SAH The Fisher scale, although deeply ingrained in neurological practice, remains a gross estimate of the amount of subarachnoid blood, and it has significant inter-observer variability This scale, currently modified (Table 26.2), emphasizes the presence or absence of a thick clot and the presence of intraventricular hemorrhage, and predicts the development of delayed cerebral ischemia.53 Another grading system was developed by Hijdra and colleagues78 (Table 26.2) A sum score TABLE 26.2 COMPUTED TOMOGRAPHY FINDINGS IN THE MODIFIED FISHER AND HIJDRA SCALE Grade Finding Focal or diffuse thin SAH without IVH Focal or diffuse thin SAH with IVH Thick SAH present without IVH Thick SAH present with IVH SAH: subarachnoid hemorrhage; IVH: intraventricular hemorrhage Data from Kistler JP, Crowell RM, Davis KR, et al The relation of cerebral vasospasm to the extent and location of subarachnoid blood visualized by CT scan: a prospective study Neurology 1983;33:424–436; and Frontera J, Claassen J, Schmidt JM, et al Prediction of symptomatic vasospasm after subarachnoid hemorrhage: the modified Fisher scale Neurosurgery 2006;59:21–27 A B C C B D D E E F Hijdra method of grading subarachnoid hemorrhage identifies 10 basal cisterns and fissures: (A) frontal interhemispheric fissure; (B) sylvian fissure, lateral parts both sides; (C) sylvian fissure, basal parts both sides; (D) suprasellar cistern both sides; (E) ambient cisterns both sides; and (F) quadrigeminal cistern The amount of blood in each cistern and fissure is graded 0, no blood; 1, small amount of blood; 2, moderately filled with blood; and 3, completely filled with blood The sum score is to 30 points.78 of greater than 20 is considered predictive of cerebral vasospasm In our recent study of different scales, we found the Hijdra scale superior to other scales in prediction of cerebral vasospasm.49 Quantification of SAH and calculation of volume may remain a useful alternative, but the applicability of this method remains unknown Grading after “resuscitation” correlates better with outcome.59 Important information can be gathered by careful inspection of CT scans The distribution of the subarachnoid blood on CT scan may suggest the location of the aneurysm, but despite subtle differences, CT scanning often cannot reliably predict the location of the aneurysm There is no correlation between the size of the aneurysm and the amount of SAH.140 Generally, patients with diffuse distribution of blood in cisterns and fissures often have a basilar artery or ACA aneurysm However, patients with a concentration of blood in the interhemispheric fissure may have an aneurysm of the anterior cerebral artery, and patients with cisternal blood surrounding the perimesencephalic cisterns most likely harbor a basilar artery aneurysm Likewise, sylvian fissure hemorrhages are mostly from an aneurysm of the MCA The additional presence of an intracerebral hematoma, however, has more localizing value Hematomas may be found in the frontal lobe (anterior communicating artery aneurysm), in the medial part of the temporal lobe (internal carotid artery aneurysm), and within the sylvian fissure extending into the temporal lobe (MCA aneurysm) (Figure 26.4).73 As alluded to earlier a benign form of SAH has been reported in which bleeding is confined to the cisterns in front of the brainstem without evidence of an aneurysm in the posterior cerebral circulation—so-called pre-truncal SAH141,142,170 (also called perimesencephalic hemorrhage)159 (Figure 26.5a) True perimesencephalic hemorrhages are purely traumatic, due to either a P2 aneurysm or spinal dural arteriovenous fistula.141,146 Typically, in these variants, blood clots not extend to the lateral sylvian fissures or to the anterior interhemispheric fissure Some extension to the basal part of the sylvian fissure is possible when CT scanning is performed very early Intraventricular hemorrhage is absent except for some sedimentation in the posterior horns Magnetic resonance imaging (MRI) is helpful in localizing the blood clot in front of the brainstem, and no cause has been found with this modality (Figure 26.5b) MRI of the cervical spine has also been unrevealing.170 http://internalmedicinebook.com (a) (a1) (b) (c) (a2) (d) (e) (f) (g) (h) FIGURE 26.4: Computed tomographic patterns of subarachnoid hemorrhage with associated hematomas indirectly localizing ruptured aneurysms Temporal lobe and sylvian fissure hematoma (a, a1) (middle cerebral artery aneurysm on CTA (a2)) Frontal hematoma (anterior cerebral artery) (b) Hematoma in cavum septum pellucidum (c) Medial temporal lobe hematoma (d) Subdural hematoma (carotid artery, mostly ophthalmic artery) (e) Corpus callosum (pericallosal artery) (f) Cerebellopontine angle hematoma with posterior inferior cerebellar artery aneurysm (g, h) http://internalmedicinebook.com (a) (b) (c) (d) (e) (f) FIGURE 26.5: Nonaneurysmal pretruncal (perimesencephalic) subarachnoid hemorrhage (a, b) Computed tomographic scan patterns of pretruncal nonaneurysmal subarachnoid hemorrhage in different patients The spectrum includes complete filling of suprasellar cisterns to more restricted clots and subtle interpeduncular hematoma The amount of blood is not critical in its recognition However, the distribution of blood is limited and should not involve the entire lateral part of the sylvian fissure or the anterior hemisphere and ventricles (c, d) Magnetic resonance imaging patterns of pretruncal nonaneurysmal subarachnoid hemorrhage Blood may involve all or part of the cisterns in front of the brainstem (e) Typical pretruncal CT pattern, but PICA aneurysm (f) proving a detailed vascular study is needed http://internalmedicinebook.com 908 Index Magnetic resonance venography (MRV), 439, 442, 443f Mallory-Weiss tears, 793, 793f hemorrhage from, 793 Malnutrition, physical signs of, 207t Manikin-based simulation, 824c Mannitol, 129, 131, 260–261, 357, 375, 400, 462, 547, 635, 776, 780 Marburg variant multiple sclerosis (MS), 523f Maternal cardiac arrest anoxic-ischemic encephalopathy after, 702 causes of (BEAU-CHOPS), 702t Mechanical Embolus Removal in Cerebral Ischemia (MERCI), 396 Mechanical ventilation, 192, 527 See also Tracheostomy controlled, 196 indications for, 191–192 modes of, 194, 195t physiologic principles and standard, 192–197 weaning from, 199–200 criteria for, 199–200, 199t extubation and, 198, 200 Medulloblastoma, 543f Meningitis, 481, 591t See also Bacterial meningitis hyponatremia in, 780 pneumococcal, 535f Meningococcal meningitis, 456 chemoprophylaxis options for, 462t Mesencephalon infarct, third-nerve palsy due to, 49f Metabolic acidosis, 774–775 causes of, 774t Metabolic alkalosis, 775 causes of, 775t Metamorphopsia, 50 Methanol, 122–123 Methicillin-resistant Staphylococcus aureus (MRSA), 810 Methotrexate, 519 Methotrexate leukoencephalopathy, 524f Methylprednisolone, 397, 510, 514 Methylprednisolone pulse therapy, 618 Metoclopramide, 210, 432 Metoprolol, 762, 764, 767 Metronidazole, 473, 474t, 808 Microdialysis, 276–277 Microdialysis catheter, 276 Micropsia, 50 Midazolam, 99c, 181–182, 328, 561 Midbrain hemorrhages, 371 Middle cerebral artery (MCA), 287–290f, 296, 384–385 aneurysm, ruptured, 318 hyperdense MCA sign, 390, 390, 389f occlusion, 301f, 384–386, 389f Miller Fisher syndrome (MFS), 590t Mini-sleep test, 608, 610 Miosis, 616, 843 Mistakes, disclosure of, 874–875 Monitoring multimodal, 309–310 of the critically ill neurologic, options in, 311f rationale for, 308–309, 309c Monitoring devices, 271 See also specific topics future directions for, 282 Monocular blindness, 43 Monro-Kellie doctrine, 250 Morphine, 185, 579 Mosquito-borne eastern equine encephalomyelitis (EEE), 482–483 Motor axonal neuropathy, acute, 587 Movement disorders, 58 clinical assessment of, 58–61 line of action in, 61–62 MR angiography See Magnetic resonance angiography (MRA) MRI See Magnetic resonance imaging (MRI) Mucosal disease, stress-related, 792c Multifocal atrial tachycardia (MAT), 764 Multiple sclerosis (MS) See also Fulminant multiple sclerosis (MS) clinical and laboratory criteria for, 526c Marburg variant, 523f Muscle strength, grading, 501, 501t, 611 Muscle weakness, 67 Mutism, 348, 519 Myasthenia gravis, 591t, 608 causes and management of deterioration in, 618–620 clinical recognition of, 608–611 diagnosis of, 608, 611 diagnostic tests in, 613t exacerbation of, 608 in-hospital deterioration in, 619 initial management of, 615–618, 615t molecular footprint of, 614c neuroimaging and laboratory tests, 611–613 outcome, 620 outcome algorithm in, 621f pharmaceutical agents with potential to aggravate, 616t respiratory failure in, 608, 610–611 seronegative, 613 Myasthenia Gravis Foundation of America, 611 Mycophenolate mofetil (CellCept), 528, 619 Mycoplasma pneumoniae, 587 Myelitis See Transverse myelitis Myelopathy, 73, 502–503 causes of, 69t treatment of, 514 Myocardial ischemia, acute, 753 Myoclonus, 58, 59t Myoclonus status epilepticus, 94–95 Myorhythmias, 58 Myxedema coma, 732 precipitating factors in, 732, 731t N-acetylcysteine (NAC), 124 Naloxone, 121, 131, 133, 186 Nasogastric tube, placement of, 209, 209f complications of, 209–210 Nasojejunal tubes, 210 Index National Institutes of Health Stroke Scale (NIHSS), 384 modified, 885t Natriuretic peptides, 778–779, 779f Near-infrared spectroscopy, 279, 281f Necrotic myelopathy, 511 Neisseria meningitides, 453 Neostigmine, 608, 612, 796 Nephrotoxicity, 619 Nerve biopsy, in GBS, 591–592 Neurocritical Care Society (NCS), 140c Neurocysticercosis, 551 Neuroendovascular procedures See Endovascular techniques Neurointensivist legitimacy of, 139–141 responsibilities of, 139–145, 141t competencies, 144 morale, 141–142, 141f procedures, 142 rounds, 144, 145t training, 144, 145c Neuroleptic malignant syndrome (NMS), 61, 832 Neurologic emergency See also specific topics assessment of, 4–6 presentations of, 3–4 principles of, 3–8 Neurologic-neurosurgical intensive care unit practice models, 147–149, 148t Neuromonitors See also Monitoring questions to consider when evaluating, 310c Neuromuscular complications in transplant medicine, 671–672 Neuromuscular respiratory failure See also Respiratory failure bedside assessment of, 82f clinical features of imminent, 82t pulmonary function tests in monitoring, 83t Neuron-specific enolase (NSE), 693 Neuropathy acute motor axonal, 592 anterior ischemic optic, 51 vasculitic, 591t Neuroradiologic procedures, interventional, 652 See also Endovascular techniques Neurosciences intensive care unit (NICU), 9, 150 See also specific topics criteria for admission, 11–12t organization and layout of, 147, 148f costs, 149, 151, 151c design, 147–149 quality control, 150, 150–152 quality improvement, 150–152, 150t staffing, 149, 149f Nicardipine, 227, 334 Nifedipine, 28 Nimodipine, 328, 566, 577 Nitroprusside, 227 909 Non-heart-beating donors (NHBDs) See also Donation after cardiac death (DCD) Maastricht classification of, 858c Nonsteroidal anti-inflammatory agents (NSAIDs), 186–187 Normoglycemia, 784–785 Nosocomial bronchopneumonia, clinical diagnosis of, 804–805 Nosocomial gastrointestinal infections, 813 antimicrobial treatment of, 808, 808t Nosocomial infections, 803 antibiotic-resistance problem and, 809–810, 812 clinical features and evaluation of, 804–805 definition of, 803 in implantable CNS devices, 808–809, 809t pneumonia, 246t, 803–804 prevalence studies of, 803 related to IV catheters, 806–807 urinary tract infections (UTIs), 807–808, 808t Nuchal rigidity, 454 Nuclear brain scan, 848 Nursing care, general, 157–166 Nutrition, 205–214 enteral, 209–211 indications for gastrostomy, 211–213 parenteral, 213–214 Nutritional needs and maintenance, 205–208 Nystagmus in acute lesions of central vestibular system, 54t central, 53, 55 peripheral vestibular and congenital, 55 positional, 55 Obesity and critical illness, 206c Obstructive hydrocephalus, acute, 532 causes and management of deterioration in, 538 clinical recognition of, 532–533 initial management of, 537–538, 538t masses causing, 533t neuroimaging and laboratory tests, 533, 535f–537f, 543–544 outcome, 539, 540f pathophysiology of, 534c Ocular bobbing, 370, 371 Ocular movements, 844 Oculogyric crises, 58–59, 60f Oculomotor palsy, 47, 371, 542 Ogilvie syndrome, causes of, 796t Omeprazole, 794, 830t Ondansetron, 629 Ophthalmologic disorders, 45t See also Visual loss Ophthalmoplegia, bilateral pseudointernuclear, 610, 610f Opiate overdose, differential diagnosis and failure to reverse coma from alleged, 133t Opiates, 121, 186–187 See also specific drugs adverse effects, 187t Optic nerve sheath, ultrasound of, 280–281 Optic nerve sheath diameter (ONSD), 280–281 910 Index Optic neuritis, 45 Optic neuropathy, anterior ischemic, 51 Oral care, 159–160 Organ donation See also Transplant medicine discussion of, 172 multistep process of, 865f Organ donation requests, 864–866 Organ donors, brain dead management of, 851–852 Organ procurement organizations (OPOs), 864–866 Oscillopsia, 53 Osmolality, 129, 218, 261, 261t, 547 effective, 218 Osmolar gap, 118, 123, 129, 881 Osmotic diuresis, 260–261, 261t, 576, 782, 784 Otitis, due to herpes zoster, 56f Otogenic brain abscesses, 469, 471 Otologic emergencies, 53, 54t, 56 Oximetry, noninvasive, 282–283 Oximetry monitoring, brain tissue, 276–277 Oxygen, brain tissue, 277c Oxygenation, cerebral clinical guide to improve, 278t Oxygenation monitoring, cerebral indications for, 276t Oxygenation parameters, monitoring of, 281 Pain, physiologic effects of, 183f Pain management, 177, 183–185 pharmaceutical agents for, 185–1187 (see also specific drugs) Palinopsia, 50 Palsy cranial nerve, 47t oculomotor, 45, 371, 542 third-nerve, 48f, 49f Pantoprazole, 399, 794 Papilledema, 439, 454, 520 Paradoxical breathing, 80, 81f Paralytic ileus See also Ileus causes of, 796t Paraneoplastic limbic encephalitis, 485 Paraneoplastic neuronal antineural antibodies and encephalitis, 485c Paraplegia acute, 68–69, 69t after aortic surgery, 680–681, 681t Parenchymal hemorrhages, 370 Parenteral nutrition, 213–214 Parinaud syndrome, 371, 532 Paroxysmal sympathetic hyperactivity, 568, 569f, 579 Patient-controlled analgesia (PCA), 185, 185c Patient hand-offs, essentials of, 12t Patient transfers and transports, in-hospital, 12t, 166 precautions before, 168t transfer out of ICU, 9–10 Penicillins, 795, 809, 810 Pentobarbital, 561 Penumbra System (PS), 396 Perched facet, 505 Percutaneous endoscopic gastrostomy (PEG), 212, 213f placement technique of, 213f Perimesencephalic hemorrhage See Pretruncal subarachnoid hemorrhage (SAH) Periodic lateralized epileptiform discharges (PLEDs), 300, 555 Periorbital edema and ecchymosis, 567f Peripherally inserted central venous catheter (PICC), 824–826 Peritumoral edema, glioblastoma with, 547f Perphenazine, 552t PERRLA (pupils equal, round, reactive to light and accommodation), 43 pH See Acid-base abnormalities and disorders Pharmacodynamics and pharmacokinetics, principles of, 829–830 Pharyngeal reflex, 844 Phencyclidine (PCP), 120 Phenobarbital, 636 Phenytoin, 97, 98, 99c, 328, 475, 557, 830t Phlebitis, 807 Phrenic nerve injury, 78–79, 85f Physical therapy in NICUs, 157, 163 See also Nursing care Pineal germinoma, 537 Pineal gland tumors, 532 Pineal parenchymal neoplasms, 537 Pineal region tumors, 532, 537 Pineoblastoma, 537, 539 Pineocytoma, 539 Pituitary apoplexy, 733–734 presenting signs of, 733, 733t pressure effects of, 733f Pituitary surgery, hyponatremia after, 780 Plasma agents, 222, 223t Plasma exchange, 527t, 596–698 adverse effects of due to IVIG and, 833 benefits of, 596 complications during and after, 597t contraindications to, 596 Plasmapheresis, 528 Plasminogen See Tissue plasminogen activator (tPA) Platelet transfusions, 819 Platinum coils, 330 detachable, 329 Pleocytosis, 507 Pleural effusions, 743–744 Pneumococcal meningitis, 535f Pneumococci, penicillin-resistant, 810 Pneumocystis carinii, 398 Pneumonia See also Aspiration pneumonia; Bronchopneumonia; Ventilator-associated pneumonia (VAP) nosocomial, 246t, 803–804 Pneumonitis See Aspiration pneumonitis Pneumothorax, 739, 743f, 723–825 Index Poisoning, coma from acid-base abnormalities and, 128–129 assessment of, 117, 118–125 changes in vital signs in, 107t laboratory studies, 126–130 mechanisms, 118c Polycythemia vera, 388, 394–395 Polymerase chain reaction (PCR), 23, 458, 489–491, 517 Polytrauma, 739 Pontine hemorrhages, 371–373, 377, 375 gastric mucosa protection in, 377 surgical options in, 378c types of, 375f Porphyria, 590 Positioning of patients, 161–163, 162f Positive end-expiratory pressure (PEEP), 600, 636, 741, 746 Positron emission tomography (PET), 544 Post-cardiac arrest syndrome, 719–720 pathophysiology, clinical manifestations, and potential treatments, 719t Posterior cerebral artery (PCA), 288 Posterior cranial fossa See Tight posterior fossa Posterior fossa epidural hematoma, 590 Posterior inferior cerebellar artery (PICA) infarct, 429 Posterior reversible encephalopathy syndrome (PRES), 519, 699f Potassium See Hyperkalemia Praziquantel, 474t Pregnancy, 698 clinical syndromes in, 698–702 general principles of the neurology of, 698 neurologic disorders of, 703t Pregnancy risk categories, FDA, 699t Pregnant patient, neurocritical care in a, 702–703 PRES (posterior reversible encephalopathy syndrome), 519, 699f Pressure-control ventilation, 196 Pressure mapping, 158, 159f Pressure-support ventilation, 196 Pressure-support weaning, 200 Pressure ulceration, 157 common areas of, 158f Pretruncal subarachnoid hemorrhage (SAH), 322, 324f Procainamide, 764 Progressive multifocal leukoencephalopathy (PML), 669, 670f Promethazine, 629 Propafenone, 764 Propanolol, 579 Propofol, 99c, 179–181, 263, 328, 447, 547, 560 Propofol infusion syndrome (PRIS), 181, 558 Propranolol, 762t Protamine sulfate, 358, 359 prothrombin complex concentrate 358, 359 Proteus mirabilis, 808 911 Proton magnetic resonance spectroscopy, 543 Pseudomonas aeruginosa, 453, 457t, 803, 810t Psychogenic status epilepticus, 94 Ptosis, 608, 609f, 610f, 611 cerebral, 385f complete, 48 Puerperum, neurologic disorders of, 703t Pulmonary disease, 739 See also specific topics Pulmonary edema, 819f acute development of, 85f neurogenic, 745, 746f clinical features and management of, 746 Pulmonary embolism, 338, 747 clinical features and management of, 747–749 Pulmonary infection score, modified, 806t Pulsatility index, 287 Pulse oximetry, 282–283 Pupil abnormalities brain death and, 843 coma and, 110, 111f, 114, 115 Pupils equal, round, reactive to light and accommodation (PERRLA), 42 Putaminal hemorrhages, 347–349, 350f Pyrazinamide, 474–475, 474t Pyridostigmine, 610, 613 Pyridoxine, 474 Pyrimethamine, 474t, 494 Q fever, 484 Quadriplegia, 595 Quantitative electroencephalography (qEEG), 298c Quinidine, 764 Rabies encephalitis, 483 “Raccoon eyes,” 567f Radial artery catheterization, 282 Radiologic landmarks, 431 See also Endovascular techniques (and complications of interventional neuroradiology) Ranitidine, 794, 795 Rapid sequence intubation, 89, 90t Rapid shallow breathing index, 200, 201f Real-time myocardial perfusion contrast echocardiography (RTP-CE), 758 Rebleeding in subarachnoid hemorrhage, 295 Reflexes, 844 brainstem reflex, 843 vestibulospinal reflex, 55 Remifentanil hydrochloride, 743 Renal replacement therapy (RRT) criteria for initiation of, 727t types of, 727f Reperfusion hemorrhage, after carotid stenting, 657f Respiration, definition of, 846 Respiratory acidosis, 775 causes of, 775t Respiratory alkalosis, 776 causes of, 776t Respiratory care, 159–160 See also specific topics 912 Index Respiratory distress, acute in mechanically ventilated patients, 740–743 algorithm for, 741f differential diagnosis of, 743t pathophysiology of, 739–740 Respiratory failure, 610–611, 613, 615 See also Neuromuscular respiratory failure acute hypercapnic, initial bedside approach to, 740t acute hypoxemic, initial bedside approach to, 740t causes of, 78–85, 79f, 80t Respiratory muscles, anatomy of, 81f Respiratory paradox See Paradoxical breathing Respiratory pulse, 80 Resuscitation medicine clinical examination of the comatose patient, 689–690 management, 691 neurology of, 688 pathophysiological concepts, 688–689 prediction of prognosis, 691–693 Retroperitoneal hematoma, 816 Reverse urea hypothesis, 728c Rhabdomyolysis, 671, 775 Richmond Agitation-Sedation Scale (RASS), 180t Rickettsial diseases, 483 Rifampin, 462t, 809 RIFLE criteria (renal failure), 722, 723t Rigidity hyperthermia and, 62c nuchal, 454 Riker Sedation-Agitation Scale (SAS), 179t RIPE therapy, 474–475 Risk prevention and the law, 875 Rituximab, 619 Rocking horse breathing See Paradoxical breathing Rocky Mountain spotted fever, 483, 484, 489 Rounds, 144, 145t Saddle anesthesia, 501 Salicylates poisoning, 123 Sedation, pharmaceutical agents for, 178–182 Sedation-Agitation Scale (SAS), 179t Seizures, 92, 301f See also Paroxysmal sympathetic hyperactivity; Status epilepticus as complication of craniotomy and biopsy, 629, 636–637 recurrent, 92 management of, 95, 97 tests, 95, 97t Seizure threshold, pharmaceutical agents that can reduce, 552t Selective serotonin reuptake inhibitors (SSRIs), 119–120 Self-fulfilling prophecy in neurocritical care, 870c Sensory ataxia, 67–68 Sensory dermatomes, 70f Sepsis catheter-related, 806 antimicrobial treatment of, 806t definition of, 709t mechanism of, 708c in NICU, 807, 808 severe, 709t Septic shock, 459 diagnostic criteria for, 709t management of, 709–711 Serratia marcescens, 808 Shivering thermoregulation and, 244c treatment options in, 247t Shock, 707 fluids and, 710c Shock index (SI), 711–712, 712f Shock states, 711–713 See also Septic shock assessment of, 707–709 Sickle-cell syndromes, 387–388 Simulation training, 142, 143c Sinus bradycardia, 762 Sinus bradycardia arrhythmia, 762 Sinusitis, 248t Sinus tachycardia, 755, 760, 761–762 Sirolimus, 519 Skin abnormalities and assessment of coma, 106t Skin care, 157–158 Skin lesions in coma, 106 Skin rash, drug-induced, 831, 832t Sodium and water homeostasis, disorders of, 776 See also Hyponatremia hypotonic and hypertonic states, 776–784 Somatosensory evoked potentials (SSEPs), 302, 304, 391, 643, 692–693, 849 Sotalol, 764 Spasm, 58 Spastic gait, 67 Spetzler-Martin grading system for arteriovenous malformations, 360t Spinal cord vascular anatomy of, 682c vascular supply of, 682c Spinal cord disorders, acute, 500 causes and management of deterioration in, 511 clinical recognition of, 500–504 diagnostic considerations in, 509t initial management of, 507–511, 510t injury mechanism in, 513c major acute spinal cord syndromes, 73t neuroimaging and laboratory tests, 504–507 outcome, 511, 514f Spinal cord injury, neurogenic bowel in, 797 Spinal cord ischemia, acute, 683t Spinal cord lesions, localizing, 70–72c Spindle coma, 302 Spinning, 53 clinical assessment of, 53–56 line of action in, 55–56 Spreading depolarization, 299c Staffing, in NICU, 149, 149 Staphylococcus aureus, 803, 812 Starling curve, 220c Statins, 830t Index Status dystonicus, 59 Status epilepticus, 92, 301f, 551 See also Convulsive status epilepticus cardiac manifestations in, 760 causes and management of deterioration in, 557–560 causes of, 94t classification of, 92–95, 93f clinical recognition of, 551–552 management of, 97–100 initial, 555–557, 556t MRI in, 554f neuroimaging and laboratory tests, 95, 552–555 EEG patterns, 96f, 297, 300–301 neuronal damage associated with, 553c nonconvulsive, 93 outcome, 560–561 presentation of, 92–95 systemic effects of, 552f treatment-refractory, 554f algorithm for, 561f Stenting, 396, 397f, 398t, 655, 657 See also Carotid artery stenting Stereotactic aspiration, 472 St Louis encephalitis, 483, 484t, 487, 492, 495 Streptococcus milleri, 472 Streptococcus pneumoniae, 388, 453, 457t, 472 Streptococcus species, 745 Stress cardiomyopathy, 328 Stress-related mucosal disease, 792c Striatocapsular infarct, 385 Striatum, 347, 348 Stroke See also Hemorrhagic stroke; Ischemic stroke acute gastrointestinal bleeding after, 793 glucose handling and, 784 EEG in, 297 following cardiac surgery, management of, 680t Subarachnoid hemorrhage (SAH), 6–7, 292–294, 319f, 320f See also Aneurysmal subarachnoid hemorrhage; Aneurysmal subarachnoid hemorrhage (SAH) electrocardiographic changes in, 755, 757f, 757t, 758f nonaneurysmal, 324f pretruncal, 322, 324f Subdural empyema and epidural abscess, empirical antibiotic therapy in, 463t Subdural/epidural ICP monitors, 271–272 Subdural hematoma, 567, 571, 574f–576f Suicide wounds, 578c Sulfadiazine, 474t, 494 Sulfamethoxazole, 474t Sulfisoxazole, 474t Superior cerebellar artery (SCA) occlusion, 429, 430c Swallowing, 209f Swallowing mechanism, abnormal features suggesting, 208t Swelling See also Edema cerebral, treatment options for, 406, 406t malignant brain swelling, 578–579 913 Synchronized intermittent-mandatory ventilation (SIMV), 194, 196 Syncope, 36 algorithm for evaluation of, 41f causes of, 38t clinical assessment of, 36–41 definition of, 36 line of action in, 38–39, 41 neurally mediated, 37 autonomic control in, 39c Syndrome of inappropriate antidiuretic hormone (SIADH), 777 Systemic inflammatory response syndrome (SIRS), diagnostic criteria for, 709t Tachycardia, 376 Tacrolimus, 522, 526, 528, 664–665 Telemedicine, 7 Temporal lobe burst hematoma, 568, 511f Terson syndrome, 319f Thalamic hematoma, 349 warfarin-associated, 355f Thalamic hemorrhage, 350f, 351f Theophylline, 795 Therapeutic hypothermia (TH), 691–693 See also Hypothermia Thermoregulation and shivering, 244c Thiamine deficiency, 207 Thioridazine, 182 Thrombin, 361 Thrombin inhibitor, 361 Thrombocytopenia, 817–819 causes of new-onset, 818t heparin-induced, 232, 818 Thromboembolic complications of neuroendovascular procedures, 654 Thromboembolic events, treatment of acute, 654 Thromboembolism, 246t prevention of, 163, 165–166 Thrombolysis, 445, 446 Thrombolytic therapy, 231, 235, 237 contraindications for, 238t Thromboplastin time, activated partial, 231 Thrombotic thrombocytopenic purpura, 388, 394 Thrombus, 749f Thunderclap headache, 25, 26, 28t Thymectomy, in myasthenia gravis, 617–620 Thymoma, 617 Thyroid, 731–733 Thyroid storm, 732–733 Thyrotoxicosis, 762–763 Tight posterior fossa, 373 Tissue plasminogen activator (tPA), 231, 360, 390, 420 Tongue bite, 93f Tonic-clonic status epilepticus, 92–93 Tonic fits, 417 Tonicity, 218 Top-of-the-basilar artery syndrome, 414, 416–417, 423 Torcular herophili, 439 914 Index Torsades de pointes, 765 Total parenteral nutrition (TPN), 213–214 formulation of, 213t Towne’s projection, 325 Toxoplasma gondii, 474 Toxoplasma infestation, 484 Toxoplasmic encephalitis, 484 T-piece usage for weaning from mechanical ventilation, 196, 200 Tracheal reflex, 844 Tracheostomy, 197–198, 503, 595 Tramadol, 327–329 Transcranial Doppler ultrasonography (TCD), 287, 444, 848–849 acute neurologic conditions, 292–296 in brain death, 296, 302–304, 848–849 general principles of, 287–292 sequential, in SAH, 294f submandibular technique, 293f temporal window technique, 287–288, 289f through occipital window, 292f through orbital window, 291f Transfers and transports of patients See Patient transfers and transports Transfusion-related acute lung injury (TRALI), 819 Transplant medicine, 663 See also Organ donation complications of CNS infections, 670–671 neuromuscular, 671–672 organ-specific, 665–670 general principles of, 663–665 Transverse myelitis, 73–74, 518, 525f, 527, 528, 591t acute, 73 causes of, 518t Trauma, 739 Trauma activation, Level 1, 4t Traumatic brain injury (TBI), 566 See also Head injury abdominal trauma and, 797 biomarkers in, 310, 311t causes and management of deterioration in, 577–579 clinical recognition of, 566–568 CT scan abnormalities in, 570t EEG in, 300 glucose handling and, 784 gunshots to head, 578c initial management of, 577t neuroimaging and laboratory tests, 568, 570–572 outcome, 579–580 transcranial Doppler in, 296 Tremor, 60, 61t Trephined, syndrome of the, 35 Triage, criteria of, 9–12 Tricyclic antidepressants, 119 Trigeminal neuralgia, refractory, 28, 33 Trimethoprim, 474t, 808 Tromethamine (THAM), 262, 576 Troponin, 766 Tuberculosis (TB), brain abscesses associated with, 475f Tuberculous (TB) meningitis, 457 Tumors of CNS See also Brain tumors WHO grading of, 545–546c Ultrasonography See Transcranial Doppler ultrasonography (TCD) Uniform Determination of Death Act, 839, 857 United Network of Organ Sharing (UNOS), 857, 864 UNOS Board of Directors recommendations, 865c Urea, 728c Urinary care, 161 Urinary tract infections (UTIs), 246t antimicrobial treatment of, 808, 808t nosocomial, 808–809, 809t Vagal spells, 760 Valproate, 97, 560, 636 Valproic acid, 433, 830t Valve surgery, complications with, 678–679 Vancomycin, 132, 461t, 462, 463, 804, 806–809, 812 Vancomycin extravasation, 834f Vaptans, 781, 782c Varicella zoster virus (VZV) encephalitis, 482, 487, 488f Vascular cannulation and procedure complications, 823–825 Vascular territories, brain, 388, 389–390f Vasculitic neuropathy 591 Vasoactive drugs commonly used for shock, 710c Vasospasm See Cerebral vasospasm Vasovagal response See Syncope Venezuelan equine encephalitis, 483 Venous access, complications associated with, 823–826 central venous catheter infection, 826 central venous catheter-related thrombosis, 825–826 manikin-based simulation of, 824c Ventilation See also Mechanical ventilation noninvasive, 196–197, 197t, 198f Ventilator, settings of, 192–193, 193f Ventilator-associated pneumonia (VAP), 803 distribution of onset of, 803–804, 804f initial antimicrobial treatment for, 806t Ventilator bundle, 194c Ventricular dysfunction, left, 753 Ventricular fibrillation, AHA consensus algorithms for, 717f Ventricular tachycardia, 765 Ventriculitis, 808–809 Ventriculostomy, 264, 274f, 336–339, 434, 435, 538, 539 Ventriculostomy-associated hemorrhage, 631, 633, 634f, 634t, 636f Verapamil, 334, 764 Vermis, LVAD-associated hemorrhage in, 679f Vertigo and otologic emergencies, 54t Very important persons (VIPs) and VIP syndrome, 170 Vestibular migraine, 57 Vestibulospinal reflexes, disorders of, 55 VIP syndrome, 170 Viral serology, 526 Visual loss, 42–44, 43c clinical assessment, 43–50 Index line of action, 50–51 crucial steps in neuro-ophthalmology, 50f Vitamin B1 (thiamine) deficiency, 207 Volume-expanding agents, 222, 223t Volume status, 218 See also Fluid replacement products and strategy clinical indicators of, 219–220, 219t Walking, impairment of, 67 clinical assessment of, 67–73 line of action in, 73–75 Wallenberg syndrome, 422, 429 Warfarin, 234–235, 448 drugs that potentiate or interfere with the action of, 235t, 830t Warfarin-associated thalamic hematoma, 355f 915 Wernicke-Korsakoff syndrome, 207 Western equine encephalomyelitis (WEE), 483, 489 West Nile encephalitis, 83 White matter disorders, acute, 518 causes and management of deterioration in, 538 clinical recognition of, 517–520 initial management of, 527t neuroimaging and laboratory tests, 520–526 outcome, 528 Wilson’s disease, dystonia in, 59 Withdrawal of care, 171–172 World Federation of Neurological Surgeons (WFNS), 295, 320 Xanthochromia, 29 in aneurysmal subarachnoid hemorrhage, 322 ... and impact on outcome Stroke 20 02; 33: 122 5– 123 2 28 Claassen J, Peery S, Kreiter KT, et al Predictors and clinical impact of epilepsy after subarachnoid hemorrhage Neurology 20 03;60 :20 8– 21 4 29 ... are based on the width of the neck and the size and location of the aneurysm Selection for coiling is often determined by location of the aneurysm in the posterior circulation, width of neck less... predict the location of the aneurysm There is no correlation between the size of the aneurysm and the amount of SAH.140 Generally, patients with diffuse distribution of blood in cisterns and fissures